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2. High mobility group box 1 orchestrates tissue regeneration via CXCR4

Author

Tirone, M, Tran, N, Ceriotti, C, Gorzanelli, A, Canepari, M, Bottinelli, R, Raucci, A, Di Maggio, S, Santiago, C, Mellado, M, Saclier, M, François, S, Careccia, G, He, M, De Marchis, F, Conti, V, Ben Larbi, S, Cuvellier, S, Casalgrandi, M, Preti, A, Chazaud, B, Al-Abed, Y, Messina, G, Sitia, G, Brunelli, S, Bianchi, M, Vénéreau, E, Tirone, Mario, Tran, Ngoc Lan, Ceriotti, Chiara, Gorzanelli, Andrea, Canepari, Monica, Bottinelli, Roberto, Raucci, Angela, Di Maggio, Stefania, Santiago, César, Mellado, Mario, Saclier, Marielle, François, Stéphanie, Careccia, Giorgia, He, Mingzhu, De Marchis, Francesco, Conti, Valentina, Ben Larbi, Sabrina, Cuvellier, Sylvain, CASALGRANDI, MAURA, Preti, Alessandro, Chazaud, Bénédicte, Al-Abed, Yousef, Messina, Graziella, Sitia, Giovanni, Brunelli, Silvia, Bianchi, Marco Emilio, Vénéreau, Emilie, Tirone, M, Tran, N, Ceriotti, C, Gorzanelli, A, Canepari, M, Bottinelli, R, Raucci, A, Di Maggio, S, Santiago, C, Mellado, M, Saclier, M, François, S, Careccia, G, He, M, De Marchis, F, Conti, V, Ben Larbi, S, Cuvellier, S, Casalgrandi, M, Preti, A, Chazaud, B, Al-Abed, Y, Messina, G, Sitia, G, Brunelli, S, Bianchi, M, Vénéreau, E, Tirone, Mario, Tran, Ngoc Lan, Ceriotti, Chiara, Gorzanelli, Andrea, Canepari, Monica, Bottinelli, Roberto, Raucci, Angela, Di Maggio, Stefania, Santiago, César, Mellado, Mario, Saclier, Marielle, François, Stéphanie, Careccia, Giorgia, He, Mingzhu, De Marchis, Francesco, Conti, Valentina, Ben Larbi, Sabrina, Cuvellier, Sylvain, CASALGRANDI, MAURA, Preti, Alessandro, Chazaud, Bénédicte, Al-Abed, Yousef, Messina, Graziella, Sitia, Giovanni, Brunelli, Silvia, Bianchi, Marco Emilio, and Vénéreau, Emilie

Abstract

Inflammation and tissue regeneration follow tissue damage, but little is known about how these processes are coordinated. High Mobility Group Box 1 (HMGB1) is a nuclear protein that, when released on injury, triggers inflammation. We previously showed that HMGB1 with reduced cysteines is a chemoattractant, whereas a disulfide bond makes it a proinflammatory cytokine. Here we report that fully reduced HMGB1 orchestrates muscle and liver regeneration via CXCR4, whereas disulfide HMGB1 and its receptors TLR4/MD-2 and RAGE (receptor for advanced glycation end products) are not involved. Injection of HMGB1 accelerates tissue repair by acting on resident muscle stem cells, hepatocytes, and infiltrating cells. The nonoxidizable HMGB1 mutant 3S, in which serines replace cysteines, promotes muscle and liver regeneration more efficiently than the wildtype protein and without exacerbating inflammation by selectively interacting with CXCR4. Overall, our results show that the reduced form of HMGB1 coordinates tissue regeneration and suggest that 3S may be used to safely accelerate healing after injury in diverse clinical contexts.

Published
2018

3. Role of High Mobility Group Box 1 (HMGB1) redox state on cardiac fibroblasts functions and tissue remodeling after myocardial infarction.

Author

RAUCCI, ANGELA, DI MAGGIO, S, DI MAGGIO, STEFANIA, RAUCCI, ANGELA, DI MAGGIO, S, and DI MAGGIO, STEFANIA

Abstract

High mobility group box 1 (HMGB1) is a nuclear factor that when secreted, is able to signal tissue damage. HMGB1 is also implicated in cardiac regeneration and remodeling after myocardial infarction (MI). The study of the redox state of its cysteines led to the identification of different redox isoforms of HMGB1, with different functions: the totally reduced form, named fully reduced HMGB1 has chemotactic effect; the partially oxidized form, disulfide HMGB1, induces cytokines expression; the sulfonyl HMGB1 is terminally oxidized and apparently inactive. The present study aims to examine the role of HMGB1 redox isoforms and the non-oxidizable mutant 3S-HMGB1 on human cardiac fibroblasts (hcFbs) functions in vitro and evaluate their effects on cardiac remodeling using a mouse model of MI. First we studied the effect of HMGB1 on hcFbs migration. We found that fully reduced HMGB1 and 3S-HMGB1, but not disulfide HMGB1, were able to induce hcFbs migration. Moreover, only the 3S-HMGB1 was not susceptible to oxidation and, indeed, its chemotactic effect was maintained also in presence of H2O2. Among the main receptors of HMGB1, hcFbs showed the membrane expression of CXCR4 but not TLR4 and RAGE. In order to investigate the contribution of CXCR4 to hcFbs migration, cells were treated with AMD3100, an inhibitor of CXCL12/CXCR4 binding, and we found that migration induced by fully reduced HMGB1 was abolished but not in response to 3S-HMGB1, demonstrating that HMGB1-induced migration of hcFbs is CXCR4-dependent. In addition, cxcr4-/- mouse embryonic fibroblasts did not migrate in response to fully reduced HMGB1 or 3S-HMGB1, confirming the previous result. HcFbs released basal levels of CXCL12 and the treatment with a blocking antibody for CXCL12 abolished migration induced by fully reduced HMGB1 but not by 3S-HMGB1 showing that 3S-HMGB1 does not require CXCL12 to bind CXCR4. Finally, biacore analysis demonstrated the higher affinity of 3S-HMGB1 for CXCR4 compared to fully reduc

Published
2016

4. Poster session 1Cell growth, differentiation and stem cells - Heart72Understanding the metabolism of cardiac progenitor cells: a first step towards controlling their proliferation and differentiation?73Expression of pw1/peg3 identifies a new cardiac adult stem cell population involved in post-myocardial infarction remodeling74Long-term stimulation of iPS-derived cardiomyocytes using optogenetic techniques to promote phenotypic changes in E-C coupling75Benefits of electrical stimulation on differentiation and maturation of cardiomyocytes from human induced pluripotent stem cells76Constitutive beta-adrenoceptor-mediated cAMP production controls spontaneous automaticity of human induced pluripotent stem cell-derived cardiomyocytes77Formation and stability of T-tubules in cardiomyocytes78Identification of miRNAs promoting human cardiomyocyte proliferation by regulating Hippo pathway79A direct comparison of foetal to adult epicardial cell activation reveals distinct differences relevant for the post-injury response80Role of neuropilins in zebrafish heart regeneration81Highly efficient immunomagnetic purification of cardiomyocytes derived from human pluripotent stem cells82Cardiac progenitor cells posses a molecular circadian clock and display large 24-hour oscillations in proliferation and stress tolerance83Influence of sirolimus and everolimus on bone marrow-derived mesenchymal stem cell biology84Endoglin is important for epicardial behaviour following cardiac injuryCell death and apoptosis - Heart87Ultrastructural alterations reflecting Ca2+ handling and cell-to-cell coupling disorders precede occurrence of severe arrhythmias in intact animal heart88Urocortin-1 promotes cardioprotection through ERK1/2 and EPAC pathways: role in apoptosis and necrosis89Expression p38 MAPK and Cas-3 in myocardium LV of rats with experimental heart failure at melatonin and enalapril introductionTranscriptional control and RNA species - Heart92Accumulation of beta-amyloid 1-40 in HF patients: the role of lncRNA BACE1-AS93Role of miR-182 in zebrafish and mouse models of Holt-Oram syndrome94Mir-27 distinctly regulates muscle-enriched transcription factors and growth factors in cardiac and skeletal muscle cells95AF risk factors impair PITX2 expression leading to Wnt-microRNA-ion channel remodelingCytokines and cellular inflammation - Heart98Post-infarct survival depends on the interplay of monocytes, neutrophils and interferon gamma in a mouse model of myocardial Infarction99Inflammatory cd11b/c cells play a protective role in compensated cardiac hypertrophy by promoting an orai3-related pro-survival signal100Anti-inflammatory effects of endothelin receptor blockade in the atrial tissue of spontaneously hypertensive rats101Mesenchymal stromal cells reduce NLRP3 inflammasome activity in Coxsackievirus B3-induced myocarditis102Mesenchymal stromal cells modulate monocytes trafficking in Coxsackievirus B3-induced myocarditis103The impact of regulatory T lymphocytes on long-term mortality in patients with chronic heart failure104Temporal dynamics of dendritic cells after ST-elevation myocardial infarction relate with improvement of myocardial functionGrowth factors and neurohormones - Heart107Preconditioning of hypertrophied heart: miR-1 and IGF-1 crosstalk108Modulation of catecholamine secretion from human adrenal chromaffin cells by manipulation of G protein-coupled receptor kinase-2 activity109Evaluation of cyclic adenosin-3,5- monophosphate and neurohormones in patients with chronic heart failureNitric oxide and reactive oxygen species - Heart112Hydrogen sulfide donor inhibits oxidative and nitrosative stress, cardiohemodynamics disturbances and restores cNOS coupling in old rats113Role and mechanisms of action of aldehydes produced by monoamine oxidase A in cardiomyocyte death and heart failure114Exercise training has contrasting effects in myocardial infarction and pressure-overload due to different endothelial nitric oxide synthase regulation115S-Nitroso Human Serum Albumin dose-dependently leads to vasodilation and alters reactive hyperaemia in coronary arteries of an isolated mouse heart model116Modulating endothelial nitric oxide synthase with folic acid attenuates doxorubicin-induced cardiomyopathy119Effects of long-term very high intensity exercise on aortic structure and function in an animal model120Electron paramagnetic resonance spectroscopy quantification of nitrosylated hemoglobin (HbNO) as an index of vascular nitric oxide bioavailability in vivo121Deletion of repressor activator protein 1 impairs acetylcholine-induced relaxation due to production of reactive oxygen speciesExtracellular matrix and fibrosis - Heart124MicroRNA-19b is associated with myocardial collagen cross-linking in patients with severe aortic stenosis. Potential usefulness as a circulating biomarker125A new ex vivo model to study cardiac fibrosis126Heterogeneity of fibrosis and fibroblast differentiation in the left ventricle after myocardial infarction127Effect of carbohydrate metabolism degree compensation to the level of galectin-3 changes in hypertensive patients with chronic heart failure and type 2 diabetes mellitus128Statin paradox in association with calcification of bicuspid aortic valve interstitial cells129Cardiac function remains impaired despite reversible cardiac fibrosis after healed experimental viral myocarditisIon channels, ion exchangers and cellular electrophysiology - Heart132Identifying a novel role for PMCA1 (Atp2b1) in heart rhythm instability133Mutations of the caveolin-3 gene as a predisposing factor for cardiac arrhythmias134The human sinoatrial node action potential: time for a computational model135iPSC-derived cardiomyocytes as a model to dissect ion current alterations of genetic atrial fibrillation136Postextrasystolic potentiation in healthy and diseased hearts: effects of the site of origin and coupling interval of the preceding extrasystole137Absence of Nav1.8-based (late) sodium current in rabbit cardiomyocytes and human iPSC-CMs138hiPSC-derived cardiomyocytes from Brugada Syndrome patients without identified mutations do not exhibit cellular electrophysiological abnormalitiesMicrocirculation141Atherogenic indices, collagen type IV turnover and the development of microvascular complications- study in diabetics with arterial hypertension142Changes in the microvasculature and blood viscosity in women with rheumatoid arthritis, hypercholesterolemia and hypertensionAtherosclerosis145Shear stress regulates endothelial autophagy: consequences on endothelial senescence and atherogenesis146Obstructive sleep apnea causes aortic remodeling in a chronic murine model147Aortic perivascular adipose tissue displays an aged phenotype in early and late atherosclerosis in ApoE-/- mice148A systematic evaluation of the cellular innate immune response during the process of human atherosclerosis149Inhibition of Coagulation factor Xa increases plaque stability and attenuates the onset and progression of atherosclerotic plaque in apolipoprotein e-deficient mice150Regulatory CD4+ T cells from patients with atherosclerosis display pro-inflammatory skewing and enhanced suppression function151Hypoxia-inducible factor (HIF)-1alpha regulates macrophage energy metabolism by mediating miRNAs152Extracellular S100A4 is a key player of smooth muscle cell phenotypic transition: implications in atherosclerosis153Microparticles of healthy origins improve atherosclerosis-associated endothelial progenitor cell dysfunction via microRNA transfer154Arterial remodeling and metabolism impairment in early atherosclerosis155Role of pannexin1 in atherosclerotic plaque formationCalcium fluxes and excitation-contraction coupling158Amphiphysin II induces tubule formation in cardiac cells159Interleukin 1 beta regulation of connexin 43 in cardiac fibroblasts and the effects of adult cardiac myocyte:fibroblast co-culture on myocyte contraction160T-tubular electrical defects contribute to blunted beta-adrenergic response in heart failure161Beat-to-beat variability of intracellular Ca2+ dynamics of Purkinje cells in the infarct border zone of the mouse heart revealed by rapid-scanning confocal microscopy162The efficacy of late sodium current blockers in hypertrophic cardiomyopathy is dependent on genotype: a study on transgenic mouse models with different mutations163Synthesis of cADPR and NAADP by intracellular CD38 in heart: role in inotropic and arrhythmogenic effects of beta-adrenoceptor signalingContractile apparatus166Towards an engineered heart tissue model of HCM using hiPSC expressing the ACTC E99K mutation167Diastolic mechanical load delays structural and functional deterioration of ultrathin adult heart slices in culture168Structural investigation of the cardiac troponin complex by molecular dynamics169Exercise training restores myocardial and oxidative skeletal muscle function from myocardial infarction heart failure ratsOxygen sensing, ischaemia and reperfusion172A novel antibody specific to full-length stromal derived factor-1 alpha reveals that remote conditioning induces its cleavage by endothelial dipeptidyl peptidase 4173Attenuation of myocardial and vascular arginase activity by vagal nerve stimulation via a mechanism involving alpha-7 nicotinic receptor during cardiac ischemia and reperfusion174Novel nanoparticle-mediated medicine for myocardial ischemia-reperfusion injury simultaneously targeting mitochondrial injury and myocardial inflammation175Acetylcholine plays a key role in myocardial ischaemic preconditioning via recruitment of intrinsic cardiac ganglia176The role of nitric oxide and VEGFR-2 signaling in post ischemic revascularization and muscle recovery in aged hypercholesterolemic mice177Efficacy of ischemic preconditioning to protect the human myocardium: the role of clinical conditions and treatmentsCardiomyopathies and fibrosis180Plakophilin-2 haploinsufficiency leads to impaired canonical Wnt signaling in ARVC patient181Improved technique for customized, easier, safer and more reliable transverse aortic arch banding and debanding in mice as a model of pressure overload hypertrophy182Late sodium current inhibitors for the treatment of inducible obstruction and diastolic dysfunction in hypertrophic cardiomyopathy: a study on human myocardium183Angiotensin II receptor antagonist fimasartan has protective role of left ventricular fibrosis and remodeling in the rat ischemic heart184Role of High-Mobility Group Box 1 (HMGB1) redox state on cardiac fibroblasts activities and heart function after myocardial infarction185Atrial remodeling in hypertrophic cardiomyopathy: insights from mouse models carrying different mutations in cTnT186Electrophysiological abnormalities in ventricular cardiomyocytes from a Maine Coon cat with hypertrophic cardiomyopathy: effects of ranolazine187ZBTB17 is a novel cardiomyopathy candidate gene and regulates autophagy in the heart188Inhibition of SRSF4 in cardiomyocytes induces left ventricular hypertrophy189Molecular characterization of a novel cardiomyopathy related desmin frame shift mutation190Autonomic characterisation of electro-mechanical remodeling in an in-vitro leporine model of heart failure191Modulation of Ca2+-regulatory function by three novel mutations in TNNI3 associated with severe infant restrictive cardiomyopathyAging194The aging impact on cardiac mesenchymal like stromal cells (S+P+)195Reversal of premature aging markers after bariatric surgery196Sex-associated differences in vascular remodeling during aging: role of renin-angiotensin system197Role of the receptor for advanced glycation end-products (RAGE) in age dependent left ventricle dysfunctionsGenetics and epigenetics200hsa-miR-21-5p as a key factor in aortic remodeling during aneurysm formation201Co-inheritance of mutations associated with arrhythmogenic and hypertrophic cardiomyopathy in two Italian families202Lamin a/c hot spot codon 190: form various amino acid substitutions to clinical effects203Treatment with aspirin and atorvastatin attenuate cardiac injury induced by rat chest irradiation: Implication of myocardial miR-1, miR-21, connexin-43 and PKCGenomics, proteomics, metabolomics, lipidomics and glycomics206Differential phosphorylation of desmin at serines 27 and 31 drives the accumulation of preamyloid oligomers in heart failure207Potential role of kinase Akt2 in the reduced recovery of type 2 diabetic hearts subjected to ischemia / reperfusion injury208A proteomics comparison of extracellular matrix remodelling in porcine coronary arteries upon stent implantationMetabolism, diabetes mellitus and obesity211Targeting grk2 as therapeutic strategy for cancer associated to diabetes212Effects of salbutamol on large arterial stiffness in patients with metabolic syndrome213Circulating microRNA-1 and microRNA-133a: potential biomarkers of myocardial steatosis in type 2 diabetes mellitus214Anti-inflammatory nutrigenomic effects of hydroxytyrosol in human adipocytes - protective mechanisms of mediterranean diets in obesity-related inflammation215Alterations in the metal content of different cardiac regions within a rat model of diabetic cardiomyopathyTissue engineering218A novel conductive patch for application in cardiac tissue engineering219Establishment of a simplified and improved workflow from neonatal heart dissociation to cardiomyocyte purification and characterization220Effects of flexible substrate on cardiomyocytes cell culture221Mechanical stretching on cardiac adipose progenitors upregulates sarcomere-related genes

Author

Andre, E, primary, Yaniz-Galende, E, primary, Hamilton, C, primary, Dusting, G J, primary, Hellen, N, primary, Poulet, CE, primary, Diez Cunado, M, primary, Smits, AM, primary, Lowe, V, primary, Eckardt, D, primary, Du Pre, B, primary, Sanz Ruiz, R, primary, Moerkamp, A T, primary, Tribulova, N, primary, Smani, T, primary, Liskova, Y V, primary, Greco, S, primary, Guzzolino, E, primary, Franco, D, primary, Lozano-Velasco, E, primary, Knorr, M, primary, Pavoine, C, primary, Bukowska, A, primary, Van Linthout, S, primary, Miteva, K, primary, Sulzgruber, P, primary, Latet, S C, primary, Portnychenko, A, primary, Cannavo, A, primary, Kamilova, U, primary, Sagach, VF, primary, Santin, Y, primary, Octavia, Y, primary, Haller, PM, primary, Rubies, C, primary, Dei Zotti, F, primary, Wong, KHK, primary, Gonzalez Miqueo, A, primary, Kruithof, BPT, primary, Kadur Nagaraju, C, primary, Shaposhnikova, Y, primary, Songia, P, primary, Lindner, D, primary, Wilson, C, primary, Benzoni, P, primary, Fabbri, A, primary, Campostrini, G, primary, Jorge, E, primary, Casini, S, primary, Mengarelli, I, primary, Nikolov, A, primary, Bublikov, DS, primary, Kheloufi, M, primary, Walker, R E, primary, Van Dijk, RA, primary, Posthuma, JJ, primary, Dumitriu, I E, primary, Karshovska, E, primary, Sakic, A, primary, Alexandru, N, primary, Martin-Lorenzo, M, primary, Molica, F, primary, Taylor, RF, primary, Mcarthur, L, primary, Crocini, C, primary, Matsuyama, T-A, primary, Mazzoni, L, primary, Lin, W K, primary, Owen, TJ, primary, Scigliano, M, primary, Sheehan, A, primary, Bezerra Gurgel, A R, primary, Bromage, DI, primary, Kiss, A, primary, Ikeda, G, primary, Pickard, J M J, primary, Wirth, G, primary, Casos, K, primary, Khudiakov, A, primary, Nistal, JF, primary, Ferrantini, C, primary, Park, S-J, primary, Di Maggio, S, primary, Gentile, F, primary, Dini, L, primary, Buyandelger, B, primary, Larrasa-Alonso, J, primary, Schirmer, I, primary, Chin, SH, primary, Cimiotti, D, primary, Martini, H, primary, Hohensinner, P J, primary, Garabito, M, primary, Zeni, F, primary, Licholai, S, primary, De Bortoli, M, primary, Sivitskaya, L, primary, Viczenczova, C, primary, Rainer, PP, primary, Smith, LE, primary, Suna, G, primary, Gambardella, J, primary, Cozma, A, primary, De Gonzalo Calvo, D, primary, Scoditti, E, primary, Clark, B J, primary, Mansfield, C, primary, Gomez, L, primary, Llucia-Valldeperas, A, primary, De Pauw, A, additional, Porporato, P, additional, Bouzin, C, additional, Draoui, N, additional, Sonveaux, P, additional, Balligand, J-L, additional, Mougenot, N, additional, Formicola, L, additional, Nadaud, S, additional, Dierick, F, additional, Hajjar, RJ, additional, Marazzi, G, additional, Sassoon, D, additional, Hulot, J-S, additional, Zamora, VR, additional, Burton, FL, additional, Macquaide, N, additional, Smith, GL, additional, Hernandez, D, additional, Sivakumaran, P, additional, Millard, R, additional, Wong, RCB, additional, Pebay, A, additional, Shepherd, RK, additional, Lim, SY, additional, Owen, T, additional, Jabbour, RJ, additional, Kloc, M, additional, Kodagoda, T, additional, Denning, C, additional, Harding, SE, additional, Ramos, S, additional, Terracciano, C, additional, Gorelik, J, additional, Wei, K, additional, Bushway, P, additional, Ruiz-Lozano, P, additional, Mercola, M, additional, Moerkamp, AT, additional, Vegh, AMD, additional, Dronkers, E, additional, Lodder, K, additional, Van Herwaarden, T, additional, Goumans, MJ, additional, Pellet-Many, C, additional, Zachary, I, additional, Noack, K, additional, Bosio, A, additional, Feyen, DAM, additional, Demkes, EJ, additional, Dierickx, PJ, additional, Doevendans, PA, additional, Vos, MA, additional, Van Veen, AAB, additional, Van Laake, LW, additional, Fernandez Santos, ME, additional, Suarez Sancho, S, additional, Fuentes Arroyo, L, additional, Plasencia Martin, V, additional, Velasco Sevillano, P, additional, Casado Plasencia, A, additional, Climent, AM, additional, Guillem, M, additional, Atienza Fernandez, F, additional, Fernandez-Aviles, F, additional, Dingenouts, CKE, additional, Kruithof, BPT, additional, Smits, AM, additional, Knezl, V, additional, Szeiffova Bacova, B, additional, Egan Benova, T, additional, Viczenczova, C, additional, Goncalvesova, E, additional, Slezak, J, additional, Calderon-Sanchez, E, additional, Diaz, I, additional, Ordonez, A, additional, Salikova, S P, additional, Zaccagnini, G, additional, Voellenkle, C, additional, Sadeghi, I, additional, Maimone, B, additional, Castelvecchio, S, additional, Gaetano, C, additional, Menicanti, L, additional, Martelli, F, additional, Hatcher, C, additional, D'aurizio, R, additional, Groth, M, additional, Baugmart, M, additional, Mercatanti, A, additional, Russo, F, additional, Mariani, L, additional, Magliaro, C, additional, Pitto, L, additional, Lozano-Velasco, E, additional, Jodar-Garcia, A, additional, Galiano-Torres, J, additional, Lopez-Navarrete, I, additional, Aranega, A, additional, Wagensteen, R, additional, Quesada, A, additional, Franco, D, additional, Finger, S, additional, Karbach, S, additional, Kossmann, S, additional, Muenzel, T, additional, Wenzel, P, additional, Keck, M, additional, Favier, S, additional, Fuand, A, additional, Atassi, F, additional, Barbier, C, additional, Lompre, AM, additional, Hulot, JS, additional, Nikonova, Y, additional, Pluteanu, F, additional, Kockskaemper, J, additional, Chilukoti, RK, additional, Wolke, C, additional, Lendeckel, U, additional, Gardemann, A, additional, Goette, A, additional, Miteva, K, additional, Pappritz, K, additional, Mueller, I, additional, El-Shafeey, M, additional, Ringe, J, additional, Tschoepe, C, additional, Van Linthout, S, additional, Koller, L, additional, Richter, B, additional, Blum, S, additional, Koprak, M, additional, Huelsmann, M, additional, Pacher, R, additional, Goliasch, G, additional, Wojta, J, additional, Niessner, A, additional, Van Herck, P L, additional, Claeys, M J, additional, Haine, S E, additional, Lenders, G D, additional, Miljoen, H P, additional, Segers, V F, additional, Vandendriescche, T R, additional, Hoymans, V Y, additional, Vrints, C J, additional, Lapikova-Bryhinska, T, additional, Gurianova, V, additional, Portnichenko, H, additional, Vasylenko, M, additional, Zapara, Y, additional, Portnichenko, V, additional, Liccardo, D, additional, Lymperopoulos, A, additional, Santangelo, M, additional, Leosco, D, additional, Koch, WJ, additional, Ferrara, N, additional, Rengo, G, additional, Alieva, T, additional, Rasulova, Z, additional, Masharipova, D, additional, Dorofeyeva, N A, additional, Drachuk, KO, additional, Sicard, P, additional, Yucel, Y, additional, Dutaur, M, additional, Vindis, C, additional, Parini, A, additional, Mialet-Perez, J, additional, Van Deel, ED, additional, De Boer, M, additional, De Waard, MC, additional, Duncker, DJ, additional, Nagel, F, additional, Inci, M, additional, Santer, D, additional, Hallstroem, S, additional, Podesser, BK, additional, Kararigas, G, additional, Kietadisorn, R, additional, Swinnen, M, additional, Duimel, H, additional, Verheyen, F, additional, Chrifi, I, additional, Brandt, MM, additional, Cheng, C, additional, Janssens, S, additional, Moens, AL, additional, Batlle, M, additional, Dantas, AP, additional, Sanz, M, additional, Sitges, M, additional, Mont, L, additional, Guasch, E, additional, Lobysheva, I, additional, Beauloye, C, additional, Vanhoutte, PM, additional, Tang, EHC, additional, Beaumont, J, additional, Lopez, B, additional, Ravassa, S, additional, Hermida, N, additional, Valencia, F, additional, Gomez-Doblas, JJ, additional, San Jose, G, additional, De Teresa, E, additional, Diez, J, additional, Van De Merbel, AF, additional, Kruithof-De Julio, M, additional, Claus, P, additional, Dries, E, additional, Angelo Singh, A, additional, Vermeulen, K, additional, Roderick, HL, additional, Sipido, KR, additional, Driesen, RB, additional, Ilchenko, I, additional, Bobronnikova, L, additional, Myasoedova, V, additional, Alamanni, F, additional, Tremoli, E, additional, Poggio, P, additional, Becher, PM, additional, Gotzhein, F, additional, Klingel, K, additional, Blankenberg, S, additional, Westermann, D, additional, Zi, M, additional, Cartwright, E, additional, Campostrini, G, additional, Bonzanni, M, additional, Milanesi, R, additional, Bucchi, A, additional, Baruscotti, M, additional, Difrancesco, D, additional, Barbuti, A, additional, Fantini, M, additional, Wilders, R, additional, Severi, S, additional, Benzoni, P, additional, Dell' Era, P, additional, Serzanti, M, additional, Olesen, MS, additional, Muneretto, C, additional, Bisleri, G, additional, Amoros-Figueras, G, additional, Raga, S, additional, Campos, B, additional, Alonso-Martin, C, additional, Rodriguez-Font, E, additional, Vinolas, X, additional, Cinca, J, additional, Guerra, JM, additional, Mengarelli, I, additional, Schumacher, CA, additional, Veldkamp, MW, additional, Verkerk, AO, additional, Remme, CA, additional, Veerman, C, additional, Guan, K, additional, Stauske, M, additional, Tan, H, additional, Barc, J, additional, Wilde, A, additional, Verkerk, A, additional, Bezzina, C, additional, Tsinlikov, I, additional, Tsinlikova, I, additional, Nicoloff, G, additional, Blazhev, A, additional, Garev, A, additional, Andrienko, AV, additional, Lychev, VG, additional, Vorobova, EN, additional, Anchugina, DA, additional, Vion, AC, additional, Hammoutene, A, additional, Poisson, J, additional, Dupont, N, additional, Souyri, M, additional, Tedgui, A, additional, Codogno, P, additional, Boulanger, CM, additional, Rautou, PE, additional, Torres, M, additional, Montserrat, JM, additional, Almendros, I, additional, Austin, C A, additional, Holt, C M, additional, Rijs, K, additional, Wezel, A, additional, Hamming, JF, additional, Kolodgie, FD, additional, Virmani, R, additional, Schaapherder, AF, additional, Lindeman, JHN, additional, Posma, JJN, additional, Van Oerle, R, additional, Spronk, HMH, additional, Ten Cate, H, additional, Dinkla, S, additional, Kaski, JC, additional, Schober, A, additional, Chaabane, C, additional, Ambartsumian, N, additional, Grigorian, M, additional, Bochaton-Piallat, ML, additional, Dragan, E, additional, Andrei, E, additional, Niculescu, L, additional, Georgescu, A, additional, Gonzalez-Calero, L, additional, Maroto, AS, additional, Martinez, PJ, additional, Heredero, A, additional, Aldamiz-Echevarria, G, additional, Vivanco, F, additional, Alvarez-Llamas, G, additional, Meens, MJ, additional, Pelli, G, additional, Foglia, B, additional, Scemes, E, additional, Kwak, BR, additional, Caldwell, JL, additional, Eisner, DA, additional, Dibb, KM, additional, Trafford, AW, additional, Chilton, L, additional, Smith, G L, additional, Nicklin, S A, additional, Coppini, R, additional, Ferrantini, C, additional, Yan, P, additional, Loew, LM, additional, Poggesi, C, additional, Cerbai, E, additional, Pavone, F S, additional, Sacconi, L, additional, Tanaka, H, additional, Ishibashi-Ueda, H, additional, Takamatsu, T, additional, Gentile, F, additional, Pioner, JM, additional, Santini, L, additional, Sartiani, L, additional, Bargelli, V, additional, Mugelli, A, additional, Maciejewska, M, additional, Bolton, E L, additional, Wang, Y, additional, O'brien, F, additional, Ruas, M, additional, Lei, M, additional, Sitsapesan, R, additional, Galione, A, additional, Terrar, D A, additional, Smith, JG, additional, Garcia, D, additional, Barriales-Villa, R, additional, Monserrat, L, additional, Marston, SB, additional, Watson, S, additional, Tkach, S, additional, Faggian, G, additional, Terracciano, C M, additional, Perbellini, F, additional, Eiros Zamora, J, additional, Papadaki, M, additional, Messer, A, additional, Marston, S, additional, Gould, I, additional, Johnston, A, additional, Dunne, M, additional, Smith, G, additional, Kemi, OJ, additional, Pillai, M, additional, Davidson, SM, additional, Yellon, DM, additional, Tratsiakovich, Y, additional, Jang, J, additional, Gonon, AT, additional, Pernow, J, additional, Matoba, T, additional, Koga, J, additional, Egashira, K, additional, Burke, N, additional, Korpisalo, P, additional, Hakkarainen, H, additional, Laidinen, S, additional, Yla-Herttuala, S, additional, Ferrer-Curriu, G, additional, Perez, M, additional, Permanyer, E, additional, Blasco-Lucas, A, additional, Gracia, JM, additional, Castro, MA, additional, Barquinero, J, additional, Galinanes, M, additional, Kostina, D, additional, Kostareva, A, additional, Malashicheva, A, additional, Merino, D, additional, Ruiz, L, additional, Gomez, J, additional, Juarez, C, additional, Gil, A, additional, Garcia, R, additional, Hurle, MA, additional, Mazzoni, L, additional, Rossi, A, additional, Tesi, C, additional, Belardinelli, L, additional, Olivotto, I, additional, Eun-Ji, EJ, additional, Lim, B-K, additional, Choi, D-J, additional, Milano, G, additional, Bertolotti, M, additional, De Marchis, F, additional, Zollo, F, additional, Sommariva, E, additional, Capogrossi, M C, additional, Pompilio, G, additional, Bianchi, M E, additional, Raucci, A, additional, Scellini, B, additional, Tardiff, J, additional, Diolaiuti, L, additional, Ferrari, P, additional, Mansfield, C, additional, Luther, P, additional, Knoell, R, additional, Villalba, M, additional, Sanchez-Cabo, F, additional, Lopez-Olaneta, MM, additional, Ortiz-Sanchez, P, additional, Garcia-Pavia, P, additional, Lara-Pezzi, E, additional, Klauke, B, additional, Gerdes, D, additional, Schulz, U, additional, Gummert, J, additional, Milting, H, additional, Wake, E, additional, Kocsis-Fodor, G, additional, Brack, KE, additional, Ng, GA, additional, Smolina, N, additional, Majchrzak, M, additional, Moehner, D, additional, Wies, A, additional, Stehle, R, additional, Pfitzer, G, additional, Muegge, A, additional, Jaquet, K, additional, Maggiorani, D, additional, Lefevre, L, additional, Cussac, D, additional, Douin-Echinard, V, additional, Ebenbauer, B, additional, Kaun, C, additional, Prager, M, additional, Rega-Kaun, G, additional, Costa, G, additional, Onetti, Y, additional, Jimenez-Altayo, F, additional, Vila, E, additional, Dantas, A P, additional, Scopece, A, additional, Piacentini, L, additional, Bianchi, ME, additional, Capogrossi, MC, additional, Colombo, G, additional, Blaz, M, additional, Kapelak, B, additional, Sanak, M, additional, Bauce, B, additional, Calore, C, additional, Lorenzon, A, additional, Calore, M, additional, Poloni, G, additional, Mazzotti, E, additional, Rigato, I, additional, Daliento, L, additional, Basso, C, additional, Thiene, G, additional, Melacini, P, additional, Corrado, D, additional, Rampazzo, A, additional, Danilenko, NG, additional, Vaikhanskaya, TG, additional, Davydenko, OG, additional, Kura, B, additional, Yin, CH, additional, Kukreja, R, additional, Tribulova, N, additional, Lee, DI, additional, Sorge, M, additional, Glabe, C, additional, Paolocci, N, additional, Guarnieri, C, additional, Tomaselli, GF, additional, Kass, DA, additional, Van Eyk, JE, additional, Agnetti, G, additional, Cordwell, SJ, additional, White, MY, additional, Wojakowski, W, additional, Lynch, M, additional, Barallobre-Barreiro, J, additional, Yin, X, additional, Mayr, U, additional, White, S, additional, Jahingiri, M, additional, Hill, J, additional, Mayr, M, additional, Sorriento, D, additional, Ciccarelli, M, additional, Fiordelisi, A, additional, Campiglia, P, additional, Trimarco, B, additional, Iaccarino, G, additional, Sitar Taut, AV, additional, Schiau, S, additional, Orasan, O, additional, Halloumi, W, additional, Negrean, V, additional, Zdrenghea, D, additional, Pop, D, additional, Van Der Meer, RW, additional, Rijzewijk, LJ, additional, Smit, JWA, additional, Revuelta-Lopez, E, additional, Nasarre, L, additional, Escola-Gil, JC, additional, Lamb, HJ, additional, Llorente-Cortes, V, additional, Pellegrino, M, additional, Massaro, M, additional, Carluccio, MA, additional, Calabriso, N, additional, Wabitsch, M, additional, Storelli, C, additional, De Caterina, R, additional, Church, S J, additional, Callagy, S, additional, Begley, P, additional, Kureishy, N, additional, Mcharg, S, additional, Bishop, P N, additional, Unwin, R D, additional, Cooper, G J S, additional, Mawad, D, additional, Tonkin, J, additional, Bello, S O, additional, Simonotto, J D, additional, Lyon, A R, additional, Stevens, M M, additional, Harding, S E, additional, Kernbach, M, additional, Czichowski, V, additional, Fuentes, L, additional, Hernandez-Redondo, I, additional, Guillem, MS, additional, Fernandez, ME, additional, Sanz, R, additional, Atienza, F, additional, Soler-Botija, C, additional, Prat-Vidal, C, additional, Galvez-Monton, C, additional, Roura, S, additional, Perea-Gil, I, additional, Bragos, R, additional, and Bayes-Genis, A, additional

Published
2016
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6. An epigenetic view on alternative splicing

Author

Di Maggio, S, Braschi, E, Fontana, G, Rigamonti, A, Barabino, S, FONTANA, GABRIELE ALESSANDRO, RIGAMONTI, AURORA, BARABINO, SILVIA MARIA LUISA, Di Maggio, S, Braschi, E, Fontana, G, Rigamonti, A, Barabino, S, FONTANA, GABRIELE ALESSANDRO, RIGAMONTI, AURORA, and BARABINO, SILVIA MARIA LUISA

Abstract

Genome-wide analysis indicate that alternative splicing of mRNA precursors (pre-mRNAs) affects the vast majority of human genes. Alternative splicing provides a fundamental mechanism to increases transcriptome complexity, allowing the production of two or more mRNA variants that often encode proteins with different, sometimes opposite functions. Its importance is underscored by the observation that misregulated alternative splicing can lead to human diseases. Pre-mRNA splicing has long been known to be regulated by cis-acting sequence elements and trans-acting protein factors. In higher eukaryotes, it mostly occurs co-transcriptionally so that it is not surprising that a role for chromatin and epigenetic factors in the regulation of exon inclusion is now emerging. In this review, we will discuss the most recent findings on the roles played by chromatin structure on the modulation of the cotranscriptional splicing reactions. In particular, we will focus our attention on how the modulation of the transcribing RNA polymerase II, the changes in nucleosome architecture and the presence of different histone modifications contribute to the regulation of the splicing process.

Published
2013

7. mHealth Technology Use and Implications in Historically Underserved and Minority Populations in the United States: Systematic Literature Review

Author

Anderson-Lewis, Charkarra, Darville, Gabrielle, Mercado, Rebeccah Eve, Howell, Savannah, and Di Maggio, Samantha

Subjects
Information technology, T58.5-58.64, Public aspects of medicine, RA1-1270
Abstract

BackgroundThe proportion of people in the United States who are members of at least two ethnic groups is projected to increase to 10% by the year 2050. This makes addressing health disparities and health inequities in minority populations increasingly more difficult. Minority populations, including those who classify themselves as African American and Hispanic, are using mobile phones to access health information via the internet more frequently than those who classify themselves as white, providing unique opportunities for those in public health and health education to reach these traditionally underserved populations using mobile health (mHealth) interventions. ObjectiveThe objective of this review was to assess studies conducted in the United States that have used mHealth tools and strategies to develop and implement interventions in underserved populations. This review also examines the ways in which mHealth strategies are being employed in public health interventions to these priority population groups, as mobile phone capabilities include text messaging, mobile apps, internet access, emails, video streaming, social media, instant messaging, and more. MethodsA systematic literature review was conducted using key search phrases, the matrix method, and Preferred Reporting Items for Systematic Reviews and Meta-Analyses flowchart diagram to identify key studies conducted between the years of 2009-2016 in the United States. These studies were reviewed for their use of mHealth interventions in historically underserved and minority populations. ResultsA total of 16,270 articles were initially identified using key search phrases in three databases. Titles were reviewed and articles not meeting criteria were excluded, leaving 156 articles for further review. After additional review for relevance and inclusion criteria, 16 articles were qualified and analyzed. ConclusionsmHealth is a promising area of development for public health and health education. While successful research has been done using text messaging (short message service, SMS) and other mHealth strategies, there is a need for more research using mobile phones and tablet applications. This literature review demonstrates mHealth technology has the ability to increase prevention and health education in health disparate communities and concludes that more specified research is needed.

Published
2018
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8. Polyvariant mutant CFTR genes in patients with chronic pancreatitis

Author

Arduino, C., Gallo, M., Alfredo Brusco, Garnerone, S., Piana, M., Di Maggio, S., Gerbino Promis, G., Ferrone, M., Angeli, A., and Gaia, E.

Subjects
Adult, Male, Chi-Square Distribution, Pancreatitis, Chronic Disease, DNA Mutational Analysis, Cystic Fibrosis Transmembrane Conductance Regulator, Humans, Female, Middle Aged, Aged
Abstract

Several authors have reported an association between mutations of the cystic fibrosis transmembrane conductance regulator gene (CFTR) and chronic pancreatitis. CFTR gene transcription and protein efficiency are influenced by two polymorphic loci, (TG)m and M470V, other than the T5 allele, whose role is already well-established. The TG11/T5 haplotype is commonly found in healthy subjects, while the TG12/T5/V470 and TG13/T5/V470 haplotypes are present in congenital bilateral absence of the vas deferens (CBAVD) patients. While the T5 allele is a mutation that is over-represented in patients with chronic pancreatitis, no data are available concerning the possible allelic preference at the other two polymorphic loci, (TG)m and M470V, in these patients. For this reason, we screened 39 patients with chronic pancreatitis for the most common CFTR mutations found so far in the Italian population; in addition, we examined the length of the polypyrimidine (poly-T) tract in intron 8, the (TG)m length and the M or V codon at position 470. CFTR mutations were found in 3 patients. Poly-T variant typing identified genotype T5/T7 in 5 patients and T5/T9 in 1 patient. Direct sequencing of intron 8 in patients with the T5 variant revealed the TG12/T5/V470//TG11/T7/V470 genotype in 5 patients and TG10/T9//TG11,T5 genotype in 1 patient. In patients with chronic pancreatitis, the T5 allele is frequently associated with TG12 and V470, a haplotype already reported in CBAVD cases and quite uncommon in healthy subjects.

9. High mobility group box 1 orchestrates tissue regeneration via CXCR4

Author

Valentina Conti, Yousef Al-Abed, Marco Bianchi, Monica Canepari, Mario Mellado, Chiara Ceriotti, Giorgia Careccia, Andrea Gorzanelli, Angela Raucci, Graziella Messina, Silvia Brunelli, Stephanie François, Marielle Saclier, Francesco De Marchis, Stefania Di Maggio, Mario Tirone, Alessandro Preti, Emilie Venereau, Roberto Bottinelli, Bénédicte Chazaud, César Santiago, Ngoc Lan Tran, Sabrina Ben Larbi, Mingzhu He, Giovanni Sitia, Sylvain Cuvellier, Maura Casalgrandi, Tirone, Mario, Tran, Ngoc Lan, Ceriotti, Chiara, Gorzanelli, Andrea, Canepari, Monica, Bottinelli, Roberto, Raucci, Angela, di Maggio, Stefania, Santiago, César, Mellado, Mario, Saclier, Marielle, François, Stéphanie, Careccia, Giorgia, He, Mingzhu, De Marchis, Francesco, Conti, Valentina, Larbi, Sabrina Ben, Cuvellier, Sylvain, Casalgrandi, Maura, Preti, Alessandro, Chazaud, Bénédicte, Al-Abed, Yousef, Messina, Graziella, Sitia, Giovanni, Brunelli, Silvia, Bianchi, Marco Emilio, Vénéreau, Emilie, Tirone, M, Tran, N, Ceriotti, C, Gorzanelli, A, Canepari, M, Bottinelli, R, Raucci, A, Di Maggio, S, Santiago, C, Mellado, M, Saclier, M, François, S, Careccia, G, He, M, De Marchis, F, Conti, V, Ben Larbi, S, Cuvellier, S, Casalgrandi, M, Preti, A, Chazaud, B, Al-Abed, Y, Messina, G, Sitia, G, Brunelli, S, Bianchi, M, and Vénéreau, E

Subjects
Male, 0301 basic medicine, Receptors, CXCR4, Immunology, chemical and pharmacologic phenomena, Inflammation, ddc:616.07, HMGB1, Article, Cell Line, Proinflammatory cytokine, RAGE (receptor), Mice, 03 medical and health sciences, medicine, Animals, Humans, Immunology and Allergy, HMGB1 Protein, Nuclear protein, Research Articles, Wound Healing, Chemotactic Factors, biology, Chemistry, Muscles, BIO/13 - BIOLOGIA APPLICATA, BIO/11 - BIOLOGIA MOLECOLARE, Liver regeneration, Liver Regeneration, Cell biology, Mice, Inbred C57BL, HEK293 Cells, 030104 developmental biology, Hepatocytes, biology.protein, TLR4, Cytokines, HMGB1, tissue regeneration, satellite cells, macrophages, CXCR4, hepaocytes, Stem cell, medicine.symptom
Abstract

Inflammation and tissue regeneration follow tissue damage, but little is known about how these processes are coordinated. Tirone et al. show that alternative redox forms of high mobility group box 1 (HMGB1), the “alarmin” signal released by damaged cells, trigger inflammation or tissue repair after injury by interacting with distinct receptors and that a nonoxidizable HMGB1 mutant promotes regeneration without exacerbating inflammation., Inflammation and tissue regeneration follow tissue damage, but little is known about how these processes are coordinated. High Mobility Group Box 1 (HMGB1) is a nuclear protein that, when released on injury, triggers inflammation. We previously showed that HMGB1 with reduced cysteines is a chemoattractant, whereas a disulfide bond makes it a proinflammatory cytokine. Here we report that fully reduced HMGB1 orchestrates muscle and liver regeneration via CXCR4, whereas disulfide HMGB1 and its receptors TLR4/MD-2 and RAGE (receptor for advanced glycation end products) are not involved. Injection of HMGB1 accelerates tissue repair by acting on resident muscle stem cells, hepatocytes, and infiltrating cells. The nonoxidizable HMGB1 mutant 3S, in which serines replace cysteines, promotes muscle and liver regeneration more efficiently than the wild-type protein and without exacerbating inflammation by selectively interacting with CXCR4. Overall, our results show that the reduced form of HMGB1 coordinates tissue regeneration and suggest that 3S may be used to safely accelerate healing after injury in diverse clinical contexts.

Published
2018

10. I reperti rinvenuti nella discarica

Author

M. Scalici, L.M. Caliò, V. Caminneci, M. Livadiotti, M.C. Parello, M.S. Rizzo, M. Scalici, A. Fino, F. Leoni, M. Albertocchi, E. Brienza, G.M. Gerogiannis, G. Parello, C. Soraci, G.L. Furcas, A. Labriola, L. Piepoli, M. Camera, R. belli, G. Vallarino, M. Cozzolino, M. Liuzzi, A. Di Meo, V. Gentile, E. di Maggio, S. Giuliano, L.M. Caliò, V. Caminneci, M. Livadiotti, M.C. Parello, M.S. Rizzo, and M. Scalici

Subjects
Agrigento, Archaeology of Sicily, Late antiquity, Roman Pottery (Archaeology), Ancient Economy
Abstract

The shrine of the so-called “Roman Temple” of Agrigentum was built between the late Republican period and the reign of Tiberius, early 1st century CE. Between the 3th and 6th centuries CE, a large midden was deposited on the East side of the shrine, almost completely burying the earlier structures. During the 2016-2017 excavations, a large portion of the archaeological deposit inside the North Portico and relevant to the Late Antique midden deposit was investigated.

Published
2017

11. Role of High Mobility Group Box 1 (HMGB1) redox state on cardiac fibroblasts functions and tissue remodeling after myocardial infarction

Author

DI MAGGIO, STEFANIA and DI MAGGIO, S

Subjects
CXCR4, fibroblasts, HMGB1, myocardial, MED/11 - MALATTIE DELL'APPARATO CARDIOVASCOLARE, infarction
Abstract

High mobility group box 1 (HMGB1) is a nuclear factor that when secreted, is able to signal tissue damage. HMGB1 is also implicated in cardiac regeneration and remodeling after myocardial infarction (MI). The study of the redox state of its cysteines led to the identification of different redox isoforms of HMGB1, with different functions: the totally reduced form, named fully reduced HMGB1 has chemotactic effect; the partially oxidized form, disulfide HMGB1, induces cytokines expression; the sulfonyl HMGB1 is terminally oxidized and apparently inactive. The present study aims to examine the role of HMGB1 redox isoforms and the non-oxidizable mutant 3S-HMGB1 on human cardiac fibroblasts (hcFbs) functions in vitro and evaluate their effects on cardiac remodeling using a mouse model of MI. First we studied the effect of HMGB1 on hcFbs migration. We found that fully reduced HMGB1 and 3S-HMGB1, but not disulfide HMGB1, were able to induce hcFbs migration. Moreover, only the 3S-HMGB1 was not susceptible to oxidation and, indeed, its chemotactic effect was maintained also in presence of H2O2. Among the main receptors of HMGB1, hcFbs showed the membrane expression of CXCR4 but not TLR4 and RAGE. In order to investigate the contribution of CXCR4 to hcFbs migration, cells were treated with AMD3100, an inhibitor of CXCL12/CXCR4 binding, and we found that migration induced by fully reduced HMGB1 was abolished but not in response to 3S-HMGB1, demonstrating that HMGB1-induced migration of hcFbs is CXCR4-dependent. In addition, cxcr4-/- mouse embryonic fibroblasts did not migrate in response to fully reduced HMGB1 or 3S-HMGB1, confirming the previous result. HcFbs released basal levels of CXCL12 and the treatment with a blocking antibody for CXCL12 abolished migration induced by fully reduced HMGB1 but not by 3S-HMGB1 showing that 3S-HMGB1 does not require CXCL12 to bind CXCR4. Finally, biacore analysis demonstrated the higher affinity of 3S-HMGB1 for CXCR4 compared to fully reduced HMGB1 or its natural ligand CXCL12. Moreover, both fully reduced HMGB1 and 3S-HMGB1 affected hcFbs-matrix adhesion in a dose dependent way, while neither disulfide HMGB1 or 3S-HMGB1 modulated pro-inflammatory cytokines levels, probably because of lack of TLR4 expression, essential for this function. In vivo experiments showed that infarcted mice receiving fully reduced HMGB1 exhibited a significant recovery of cardiac function while treatment with 3S-HMGB1 determined an increase in LV dilation and infarct size and a worsening in LV function, compared to the vehicle. Finally, only fully reduced HMGB1-treated mice presented a thicker wall of the infarcted area, no sign of cardiomyocytes hypertrophy and increased arteriole density. Our results demonstrated that HMGB1-induced migration of hcFbs is CXCR4 dependent and 3S-HMGB1 does not require CXCL12 to bind the receptor, unlike fully reduced HMGB1. Moreover, the 3S-HMGB1 is active also in oxidizing conditions that may occur soon after MI. Whether these are the reasons for the 3S-HMGB1-dependent worsening of the infarcted heart function observed in vivo has to be determined.

Published
2016

12. The Mouse-Specific Splice Variant mRAGE_v4 Encodes a Membrane-Bound RAGE That Is Resistant to Shedding and Does Not Contribute to the Production of Soluble RAGE

Author

Matteo Bertolotti, Angela Raucci, Günter Fritz, Marco Bianchi, Jaron Liu, Elena Gatti, Stefania Di Maggio, Di Maggio, S, Gatti, E, Liu, J, Bertolotti, M, Fritz, G, Bianchi, MARCO EMILIO, and Raucci, A.

Subjects
0301 basic medicine, Gene isoform, Genetics, Messenger RNA, Multidisciplinary, endocrine system diseases, ADAM10, Alternative splicing, lcsh:R, nutritional and metabolic diseases, lcsh:Medicine, Biology, Primary transcript, Transmembrane protein, Cell biology, 03 medical and health sciences, Exon, 030104 developmental biology, cardiovascular system, lcsh:Q, cardiovascular diseases, Receptor, lcsh:Science, human activities
Abstract

The receptor for advanced glycation end-products (RAGE) is involved in the onset and progression of several inflammatory diseases. The RAGE primary transcript undergoes numerous alternative splicing (AS) events, some of which are species-specific. Here, we characterize the mouse-specific mRAGE_v4 splice variant, which is conserved in rodents and absent in primates. mRAGE_v4 derives from exon 9 skipping and encodes a receptor (M-RAGE) that lacks 9 amino acids between the transmembrane and the immunoglobulin (Ig) domains. RNA-Seq data confirm that in mouse lung mRAGE_v4 is the most abundant RAGE mRNA isoform after mRAGE, which codes for full-length RAGE (FL-RAGE), while in heart all RAGE variants are almost undetectable. The proteins M-RAGE and FL-RAGE are roughly equally abundant in mouse lung. Contrary to FL-RAGE, M-RAGE is extremely resistant to shedding because it lacks the peptide motif recognized by both ADAM10 and MMP9, and does not contribute significantly to soluble cRAGE formation. Thus, a cassette exon in RAGE corresponds to a specific function of the RAGE protein-the ability to be shed. Given the differences in RAGE AS variants between rodents and humans, caution is due in the interpretation of results obtained in mouse models of RAGE-dependent human pathologies.

Published
2016

13. Optical Performance Evaluation of DSSC-integrated Glassblocks for Active Building Façades

Author

Buscemi, Alessandro, Calabrò, Claudia, Corrao, Rossella, Di Maggio, Maria Sara, Morini, Marco, Pastore, Luisa, Buscemi, A., Calabrò, C., Corrao, R., Di Maggio, S., Morini, M., and Pastore, L.

Subjects
Zemax software, Glass block, BIPV, Optical analyses, Settore ICAR/10 - Architettura Tecnica, DSSC, Glassblock, BIPV, Optical analyses, DSSC, Zemax software
Abstract

The paper outlines the results of a research, carried out at the University of Palermo, aimed at the assessment of the energy performance of a novel glassblock integrated with 3rd generation Dye-Sensitized Solar Cells (DSSC), which, when installed into panels, allows obtaining translucent building envelopes able to provide high thermal and visual comfort levels while producing clean energy. The paper focuses on the optical analyses of four different configurations of DSSC-integrated glassblocks, carried out by using the optical design software Zemax. The values of optical transmittance, the solar factor and the electric power – calculated for each configuration – are discussed.

Published
2015

14. An epigenetic view on alternative splicing

Author

FONTANA, GABRIELE ALESSANDRO, RIGAMONTI, AURORA, BARABINO, SILVIA MARIA LUISA, Di Maggio, S, Braschi, E, Fontana, G, Rigamonti, A, and Barabino, S

Subjects
Chromatin, alternative splicing
Abstract

Genome-wide analysis indicate that alternative splicing of mRNA precursors (pre-mRNAs) affects the vast majority of human genes. Alternative splicing provides a fundamental mechanism to increases transcriptome complexity, allowing the production of two or more mRNA variants that often encode proteins with different, sometimes opposite functions. Its importance is underscored by the observation that misregulated alternative splicing can lead to human diseases. Pre-mRNA splicing has long been known to be regulated by cis-acting sequence elements and trans-acting protein factors. In higher eukaryotes, it mostly occurs co-transcriptionally so that it is not surprising that a role for chromatin and epigenetic factors in the regulation of exon inclusion is now emerging. In this review, we will discuss the most recent findings on the roles played by chromatin structure on the modulation of the cotranscriptional splicing reactions. In particular, we will focus our attention on how the modulation of the transcribing RNA polymerase II, the changes in nucleosome architecture and the presence of different histone modifications contribute to the regulation of the splicing process.

Published
2013

15. Abnormalities of the oculomotor function in type 1 diabetes and diabetic neuropathy.

Author

D'Addio F, Pastore I, Loretelli C, Valderrama-Vasquez A, Usuelli V, Assi E, Mameli C, Macedoni M, Maestroni A, Rossi A, Lunati ME, Morpurgo PS, Gandolfi A, Montefusco L, Bolla AM, Ben Nasr M, Di Maggio S, Melzi L, Staurenghi G, Secchi A, Bianchi Marzoli S, Zuccotti G, and Fiorina P

Subjects
Cohort Studies, Humans, Pursuit, Smooth, Saccades, Diabetes Mellitus, Type 1 complications, Diabetic Neuropathies diagnosis, Diabetic Neuropathies etiology
Abstract

Aims: Abnormalities in the oculomotor system may represent an early sign of diabetic neuropathy and are currently poorly studied. We designed an eye-tracking-based test to evaluate oculomotor function in patients with type 1 diabetes., Methods: We used the SRLab-Tobii TX300 Eye tracker®, an eye-tracking device, coupled with software that we developed to test abnormalities in the oculomotor system. The software consists of a series of eye-tracking tasks divided into 4 classes of parameters (Resistance, Wideness, Pursuit and Velocity) to evaluate both smooth and saccadic movement in different directions. We analyzed the oculomotor system in 34 healthy volunteers and in 34 patients with long-standing type 1 diabetes., Results: Among the 474 parameters analyzed with the eye-tracking-based system, 11% were significantly altered in patients with type 1 diabetes (p < 0.05), with a higher proportion of abnormalities observed in the Wideness (24%) and Resistance (10%) parameters. Patients with type 1 diabetes without diabetic neuropathy showed more frequently anomalous measurements in the Resistance class (p = 0.02). The classes of Velocity and Pursuit were less frequently altered in patients with type 1 diabetes as compared to healthy subjects, with anomalous measurements mainly observed in patients with diabetic neuropathy., Conclusions: Abnormalities in oculomotor system function can be detected in patients with type 1 diabetes using a novel eye-tracking-based test. A larger cohort study may further determine thresholds of normality and validate whether eye-tracking can be used to non-invasively characterize early signs of diabetic neuropathy., Trial: NCT04608890., (© 2022. The Author(s).)

Published
2022
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16. PD-1 blockade counteracts post-COVID-19 immune abnormalities and stimulates the anti-SARS-CoV-2 immune response.

Author

Loretelli C, Abdelsalam A, D'Addio F, Ben Nasr M, Assi E, Usuelli V, Maestroni A, Seelam AJ, Ippolito E, Di Maggio S, Loreggian L, Radovanovic D, Vanetti C, Yang J, El Essawy B, Rossi A, Pastore I, Montefusco L, Lunati ME, Bolla AM, Biasin M, Antinori S, Santus P, Riva A, Zuccotti GV, Galli M, Rusconi S, and Fiorina P

Subjects
B7-H1 Antigen immunology, CD4-Positive T-Lymphocytes drug effects, CD4-Positive T-Lymphocytes immunology, CD8-Positive T-Lymphocytes drug effects, CD8-Positive T-Lymphocytes immunology, COVID-19 immunology, Case-Control Studies, Cytokines drug effects, DNA Methylation, Female, Humans, Immunophenotyping, In Vitro Techniques, Interleukin 1 Receptor Antagonist Protein drug effects, Interleukin 1 Receptor Antagonist Protein immunology, Interleukin-1beta drug effects, Interleukin-1beta immunology, Interleukin-8 drug effects, Interleukin-8 immunology, Male, MicroRNAs metabolism, Middle Aged, Programmed Cell Death 1 Receptor antagonists & inhibitors, Promoter Regions, Genetic, Post-Acute COVID-19 Syndrome, COVID-19 complications, Cytokines immunology, Immune Checkpoint Inhibitors pharmacology, Programmed Cell Death 1 Receptor immunology, SARS-CoV-2 immunology, T-Lymphocytes drug effects, T-Lymphocytes immunology
Abstract

A substantial proportion of patients who have recovered from coronavirus disease-2019 (COVID-19) experience COVID-19-related symptoms even months after hospital discharge. We extensively immunologically characterized patients who recovered from COVID-19. In these patients, T cells were exhausted, with increased PD-1+ T cells, as compared with healthy controls. Plasma levels of IL-1β, IL-1RA, and IL-8, among others, were also increased in patients who recovered from COVID-19. This altered immunophenotype was mirrored by a reduced ex vivo T cell response to both nonspecific and specific stimulation, revealing a dysfunctional status of T cells, including a poor response to SARS-CoV-2 antigens. Altered levels of plasma soluble PD-L1, as well as of PD1 promoter methylation and PD1-targeting miR-15-5p, in CD8+ T cells were also observed, suggesting abnormal function of the PD-1/PD-L1 immune checkpoint axis. Notably, ex vivo blockade of PD-1 nearly normalized the aforementioned immunophenotype and restored T cell function, reverting the observed post-COVID-19 immune abnormalities; indeed, we also noted an increased T cell-mediated response to SARS-CoV-2 peptides. Finally, in a neutralization assay, PD-1 blockade did not alter the ability of T cells to neutralize SARS-CoV-2 spike pseudotyped lentivirus infection. Immune checkpoint blockade ameliorates post-COVID-19 immune abnormalities and stimulates an anti-SARS-CoV-2 immune response.

Published
2021
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17. The Janus face of HMGB1 in heart disease: a necessary update.

Author

Raucci A, Di Maggio S, Scavello F, D'Ambrosio A, Bianchi ME, and Capogrossi MC

Subjects
Alarmins metabolism, Animals, Biomarkers metabolism, Heart Diseases metabolism, Humans, Myocardial Infarction metabolism, Myocardial Infarction pathology, Myocarditis metabolism, Myocarditis pathology, Oxidative Stress, Reactive Oxygen Species metabolism, HMGB1 Protein metabolism, Heart Diseases pathology
Abstract

High mobility group box 1 (HMGB1) is a ubiquitous nuclear protein involved in transcription regulation, DNA replication and repair and nucleosome assembly. HMGB1 is passively released by necrotic tissues or actively secreted by stressed cells. Extracellular HMGB1 acts as a damage-associated molecular pattern (DAMPs) molecule and gives rise to several redox forms that by binding to different receptors and interactors promote a variety of cellular responses, including tissue inflammation or regeneration. Inhibition of extracellular HMGB1 in experimental models of myocardial ischemia/reperfusion injury, myocarditis, cardiomyopathies induced by mechanical stress, diabetes, bacterial infection or chemotherapeutic drugs reduces inflammation and is protective. In contrast, administration of HMGB1 after myocardial infarction induced by permanent coronary artery ligation ameliorates cardiac performance by promoting tissue regeneration. HMGB1 decreases contractility and induces hypertrophy and apoptosis in cardiomyocytes, stimulates cardiac fibroblast activities, and promotes cardiac stem cell proliferation and differentiation. Interestingly, maintenance of appropriate nuclear HMGB1 levels protects cardiomyocytes from apoptosis by preventing DNA oxidative stress, and mice with HMGB1cardiomyocyte-specific overexpression are partially protected from cardiac damage. Finally, higher levels of circulating HMGB1 are associated to human heart diseases. Hence, during cardiac injury, HMGB1 elicits both harmful and beneficial responses that may in part depend on the generation and stability of the diverse redox forms, whose specific functions in this context remain mostly unexplored. This review summarizes recent findings on HMGB1 biology and heart dysfunctions and discusses the therapeutic potential of modulating its expression, localization, and oxidative-dependent activities.

Published
2019
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18. High mobility group box 1 orchestrates tissue regeneration via CXCR4.

Author

Tirone M, Tran NL, Ceriotti C, Gorzanelli A, Canepari M, Bottinelli R, Raucci A, Di Maggio S, Santiago C, Mellado M, Saclier M, François S, Careccia G, He M, De Marchis F, Conti V, Ben Larbi S, Cuvellier S, Casalgrandi M, Preti A, Chazaud B, Al-Abed Y, Messina G, Sitia G, Brunelli S, Bianchi ME, and Vénéreau E

Subjects
Animals, Cell Line, Chemotactic Factors metabolism, Cytokines metabolism, HEK293 Cells, Hepatocytes metabolism, Hepatocytes physiology, Humans, Inflammation metabolism, Male, Mice, Mice, Inbred C57BL, Wound Healing physiology, HMGB1 Protein metabolism, Liver Regeneration physiology, Muscles metabolism, Muscles physiology, Receptors, CXCR4 metabolism
Abstract

Inflammation and tissue regeneration follow tissue damage, but little is known about how these processes are coordinated. High Mobility Group Box 1 (HMGB1) is a nuclear protein that, when released on injury, triggers inflammation. We previously showed that HMGB1 with reduced cysteines is a chemoattractant, whereas a disulfide bond makes it a proinflammatory cytokine. Here we report that fully reduced HMGB1 orchestrates muscle and liver regeneration via CXCR4, whereas disulfide HMGB1 and its receptors TLR4/MD-2 and RAGE (receptor for advanced glycation end products) are not involved. Injection of HMGB1 accelerates tissue repair by acting on resident muscle stem cells, hepatocytes, and infiltrating cells. The nonoxidizable HMGB1 mutant 3S, in which serines replace cysteines, promotes muscle and liver regeneration more efficiently than the wild-type protein and without exacerbating inflammation by selectively interacting with CXCR4. Overall, our results show that the reduced form of HMGB1 coordinates tissue regeneration and suggest that 3S may be used to safely accelerate healing after injury in diverse clinical contexts., (© 2018 Tirone et al.)

Published
2018
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19. Non-oxidizable HMGB1 induces cardiac fibroblasts migration via CXCR4 in a CXCL12-independent manner and worsens tissue remodeling after myocardial infarction.

Author

Di Maggio S, Milano G, De Marchis F, D'Ambrosio A, Bertolotti M, Palacios BS, Badi I, Sommariva E, Pompilio G, Capogrossi MC, and Raucci A

Subjects
Female, Fibroblasts pathology, Humans, Male, Myocardial Infarction pathology, Myocardium pathology, Oxidation-Reduction, Cell Movement, Chemokine CXCL12 metabolism, Fibroblasts metabolism, HMGB1 Protein metabolism, Myocardial Infarction metabolism, Myocardium metabolism, Receptors, CXCR4 metabolism
Abstract

Myocardial infarction (MI) is a major health burden worldwide. Extracellular High mobility group box 1 (HMGB1) regulates tissue healing after injuries. The reduced form of HMGB1 (fr-HMGB1) exerts chemotactic activity by binding CXCL12 through CXCR4, while the disulfide form, (ds-HMGB1), induces cytokines expression by TLR4. Here, we assessed the role of HMGB1 redox forms and the non-oxidizable mutant (3S) on human cardiac fibroblast (hcFbs) functions and cardiac remodeling after infarction. Among HMGB1 receptors, hcFbs express CXCR4. Fr-HMGB1 and 3S, but not ds-HMGB1, promote hcFbs migration through Src activation, while none of HMGB1 redox forms induces proliferation or inflammatory mediators. 3S is more effective than fr-HMGB1 in stimulating hcFbs migration and Src phosphorylation being active at lower concentrations and in oxidizing conditions. Notably, chemotaxis toward both proteins is CXCR4-dependent but, in contrast to fr-HMGB1, 3S does not require CXCL12 since hcFbs migration persists in the presence of the CXCL12/CXCR4 inhibitor AMD3100 or an anti-CXCL12 antibody. Interestingly, 3S interacts with CXCR4 and induces a different receptor conformation than CXCL12. Mice undergoing MI and receiving 3S exhibit adverse LV remodeling owing to an excessive collagen deposition promoted by a higher number of myofibroblasts. On the contrary, fr-HMGB1 ameliorates cardiac performance enhancing neoangiogenesis and reducing the infarcted area and fibrosis. Altogether, our results demonstrate that non-oxidizable HMGB1 induce a sustained cardiac fibroblasts migration despite the redox state of the environment and by altering CXCL12/CXCR4 axis. This affects proper cardiac remodeling after an infarction., (Copyright © 2017 Elsevier B.V. All rights reserved.)

Published
2017
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20. The shedding-derived soluble receptor for advanced glycation endproducts sustains inflammation during acute Pseudomonas aeruginosa lung infection.

Author

Antonelli A, Di Maggio S, Rejman J, Sanvito F, Rossi A, Catucci A, Gorzanelli A, Bragonzi A, Bianchi ME, and Raucci A

Subjects
ADAM10 Protein metabolism, Animals, Glycation End Products, Advanced metabolism, Inflammation microbiology, Mice, Mice, Inbred C57BL, Neutrophils metabolism, Inflammation metabolism, Lung metabolism, Lung microbiology, Pseudomonas Infections metabolism, Pseudomonas Infections microbiology, Pseudomonas aeruginosa pathogenicity, Receptor for Advanced Glycation End Products metabolism
Abstract

Background: The membrane-bound isoform of the receptor for advanced glycation end products (FL-RAGE) is primarily expressed by alveolar epithelial cells and undergoes shedding by the protease ADAM10, giving rise to soluble cleaved RAGE (cRAGE). RAGE has been associated with the pathogenesis of several acute and chronic lung disorders. Whether the proteolysis of FL-RAGE is altered by a given inflammatory stimulus is unknown. Pseudomonas aeruginosa causes nosocomial infections in hospitalized patients and is the major pathogen associated with chronic lung diseases., Methods: P. aeruginosa was injected in Rage-/- and wild-type mice and the impact on RAGE expression and shedding, levels of inflammation and bacterial growth was determined., Results: Acute P. aeruginosa lung infection in mice induces a reduction of the active form of ADAM10, which determines an increase of FL-RAGE expression on alveolar cells and a concomitant decrease of pulmonary cRAGE levels. This was associated with massive recruitment of leukocytes and release of pro-inflammatory factors, tissue damage and relocation of cRAGE in the alveolar and bronchial cavities. The administration of sRAGE worsened bacterial burden and neutrophils infiltration. RAGE genetic deficiency reduced the susceptibility to P. aeruginosa infection, mitigating leukocyte recruitment, inflammatory molecules production, and bacterial growth., Conclusions: These data are the first to suggest that inhibition of FL-RAGE shedding, by affecting the FL-RAGE/cRAGE levels, is a novel mechanism for controlling inflammation to acute P. aeruginosa pneumonia. sRAGE in the alveolar space sustains inflammation in this setting., General Significance: RAGE shedding may determine the progression of inflammatory lung diseases., (Copyright © 2016 Elsevier B.V. All rights reserved.)

Published
2017
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21. The Mouse-Specific Splice Variant mRAGE&#95;v4 Encodes a Membrane-Bound RAGE That Is Resistant to Shedding and Does Not Contribute to the Production of Soluble RAGE.

Author

Di Maggio S, Gatti E, Liu J, Bertolotti M, Fritz G, Bianchi ME, and Raucci A

Abstract

The receptor for advanced glycation end-products (RAGE) is involved in the onset and progression of several inflammatory diseases. The RAGE primary transcript undergoes numerous alternative splicing (AS) events, some of which are species-specific. Here, we characterize the mouse-specific mRAGE&#95;v4 splice variant, which is conserved in rodents and absent in primates. mRAGE&#95;v4 derives from exon 9 skipping and encodes a receptor (M-RAGE) that lacks 9 amino acids between the transmembrane and the immunoglobulin (Ig) domains. RNA-Seq data confirm that in mouse lung mRAGE&#95;v4 is the most abundant RAGE mRNA isoform after mRAGE, which codes for full-length RAGE (FL-RAGE), while in heart all RAGE variants are almost undetectable. The proteins M-RAGE and FL-RAGE are roughly equally abundant in mouse lung. Contrary to FL-RAGE, M-RAGE is extremely resistant to shedding because it lacks the peptide motif recognized by both ADAM10 and MMP9, and does not contribute significantly to soluble cRAGE formation. Thus, a cassette exon in RAGE corresponds to a specific function of the RAGE protein-the ability to be shed. Given the differences in RAGE AS variants between rodents and humans, caution is due in the interpretation of results obtained in mouse models of RAGE-dependent human pathologies., Competing Interests: The authors have declared that no competing interests exist.

Published
2016
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