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11. Lack of ApoA-I in ApoEKO Mice Causes Skin Xanthomas, Worsening of Inflammation, and Increased Coronary Atherosclerosis in the Absence of Hyperlipidemia

Author

Busnelli, Marco, primary, Manzini, Stefano, additional, Colombo, Alice, additional, Franchi, Elsa, additional, Bonacina, Fabrizia, additional, Chiara, Matteo, additional, Arnaboldi, Francesca, additional, Donetti, Elena, additional, Ambrogi, Federico, additional, Oleari, Roberto, additional, Lettieri, Antonella, additional, Horner, David, additional, Scanziani, Eugenio, additional, Norata, Giuseppe Danilo, additional, and Chiesa, Giulia, additional

Published
2022
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17. Identification and Characterization of Human Observational Studies in Nutritional Epidemiology on Gut Microbiomics for Joint Data Analysis

Author

Pinart, Mariona, primary, Nimptsch, Katharina, additional, Forslund, Sofia K., additional, Schlicht, Kristina, additional, Gueimonde, Miguel, additional, Brigidi, Patrizia, additional, Turroni, Silvia, additional, Ahrens, Wolfgang, additional, Hebestreit, Antje, additional, Wolters, Maike, additional, Dötsch, Andreas, additional, Nöthlings, Ute, additional, Oluwagbemigun, Kolade, additional, Cuadrat, Rafael R. C., additional, Schulze, Matthias B., additional, Standl, Marie, additional, Schloter, Michael, additional, De Angelis, Maria, additional, Iozzo, Patricia, additional, Guzzardi, Maria Angela, additional, Vlaemynck, Geertrui, additional, Penders, John, additional, Jonkers, Daisy M. A. E., additional, Stemmer, Maya, additional, Chiesa, Giulia, additional, Cavalieri, Duccio, additional, De Filippo, Carlotta, additional, Ercolini, Danilo, additional, De Filippis, Francesca, additional, Ribet, David, additional, Achamrah, Najate, additional, Tavolacci, Marie-Pierre, additional, Déchelotte, Pierre, additional, Bouwman, Jildau, additional, Laudes, Matthias, additional, and Pischon, Tobias, additional

Published
2021
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19. Dose-Related Effects of Repeated ETC-216 (Recombinant Apolipoprotein A-IMilano/1-Palmitoyl-2-Oleoyl Phosphatidylcholine Complexes) Administrations on Rabbit Lipid-Rich Soft Plaques: In Vivo Assessment by Intravascular Ultrasound and Magnetic Resonance Imaging

Author

Parolini, Cinzia, Marchesi, Marta, Lorenzon, Paolo, Castano, Mauro, Balconi, Elena, Miragoli, Luigi, Chaabane, Linda, Morisetti, Alberto, Lorusso, Vito, Martin, Bradley J., Bisgaier, Charles L., Krause, Brian, Newton, Roger S., Sirtori, Cesare R., and Chiesa, Giulia

Published
2008
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22. The Gut Microbiota Affects Host Pathophysiology as an Endocrine Organ: A Focus on Cardiovascular Disease

Author

Busnelli, Marco, Manzini, Stefano, and Chiesa, Giulia

Subjects
bile acids, Neurotransmitter Agents, gut microbiota, hormones, lcsh:TX341-641, Review, Fatty Acids, Volatile, digestive system, Choline, Diet, Gastrointestinal Microbiome, Bile Acids and Salts, scfa, neurohormones, Cardiovascular Diseases, Risk Factors, cardiovascular disease, Endocrine Glands, Animals, Humans, atherosclerosis, metabolism, lcsh:Nutrition. Foods and food supply
Abstract

It is widely recognized that the microorganisms inhabiting our gastrointestinal tract—the gut microbiota—deeply affect the pathophysiology of the host. Gut microbiota composition is mostly modulated by diet, and gut microorganisms communicate with the different organs and tissues of the human host by synthesizing hormones and regulating their release. Herein, we will provide an updated review on the most important classes of gut microbiota-derived hormones and their sensing by host receptors, critically discussing their impact on host physiology. Additionally, the debated interplay between microbial hormones and the development of cardiovascular disease will be thoroughly analysed and discussed.

Published
2019

25. Fat‐Shaped Microbiota Affects Lipid Metabolism, Liver Steatosis, and Intestinal Homeostasis in Mice Fed a Low‐Protein Diet

Author

Busnelli, Marco, primary, Manzini, Stefano, additional, Jablaoui, Amin, additional, Bruneau, Aurélia, additional, Kriaa, Aïcha, additional, Philippe, Catherine, additional, Arnaboldi, Francesca, additional, Colombo, Alice, additional, Ferrari, Benedetta, additional, Ambrogi, Federico, additional, Maguin, Emmanuelle, additional, Rhimi, Moez, additional, Chiesa, Giulia, additional, and Gérard, Philippe, additional

Published
2020
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26. Fenretinide treatment accelerates atherosclerosis development in apoE‐deficient mice in spite of beneficial metabolic effects

Author

Busnelli, Marco, primary, Manzini, Stefano, additional, Bonacina, Fabrizia, additional, Soldati, Sabina, additional, Barbieri, Silvia Stella, additional, Amadio, Patrizia, additional, Sandrini, Leonardo, additional, Arnaboldi, Francesca, additional, Donetti, Elena, additional, Laaksonen, Reijo, additional, Paltrinieri, Saverio, additional, Scanziani, Eugenio, additional, and Chiesa, Giulia, additional

Published
2019
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27. Myocardial overexpression of ANKRD1 causes sinus venosus defects and progressive diastolic dysfunction

Author

Piroddi, Nicoletta, primary, Pesce, Paola, primary, Scellini, Beatrice, primary, Manzini, Stefano, primary, Ganzetti, Giulia S, primary, Badi, Ileana, primary, Menegollo, Michela, primary, Cora, Virginia, primary, Tiso, Simone, primary, Cinquetti, Raffaella, primary, Monti, Laura, primary, Chiesa, Giulia, primary, Bleyl, Steven B, primary, Busnelli, Marco, primary, Dellera, Federica, primary, Bruno, Daniele, primary, Caicci, Federico, primary, Grimaldi, Annalisa, primary, Taramelli, Roberto, primary, Manni, Lucia, primary, Sacerdoti, David, primary, Tesi, Chiara, primary, Poggesi, Corrado, primary, Ausoni, Simonetta, primary, Acquati, Francesco, primary, and Campione, Marina, primary

Published
2019
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38. Management of lipoprotein-X accumulation in severe cholestasis by semi-selective LDL-apheresis

Author

Franceschini, Guido, Busnach, Ghil, Chiesa, Giulia, and Sirtori, Cesare R.

Subjects
Lipoproteins -- Physiological aspects, Liver failure -- Causes of, Cholestasis -- Care and treatment, Cholestasis -- Complications, Apheresis -- Evaluation, Health, Health care industry
Abstract

Liver disorders characterized by prolonged bile stasis are often associated with the accumulation of an abnormal lipoprotein, lipoprotein-X (LP-X), in plasma. LP-X is separated in the low-density lipoprotein (LDL) density range, but lacks apoliprotein B and does not interact with the LDL receptor; LP-X can cause hyperlipidemia, cutaneous xanthomas, and worsening of arterial disease. We report the case of a patient with severe cholestasis, markedly elevated plasma cholesterol levesl (26.8 to 31.5 mmol/L), mainly due to a massive accumulation of LP-X in plasma, and diffuse xanthomas. To reduce the elevated cholesterol levels, the patient was given extracorporeal treatment aimed at removing atherogenic lipoprotein (LDL-apheresis). LDL-apheresis was performed at weekly or bi-weekly intervals, either by a semi-selective technique using filters with a defined pore diameter (double filtration, DF) or by a more selective technique using dextran-sulfate-cellulose (DSC) columns able to bind LDL. The semi-selective DF technique proved more effective than DSC, removing 48% of total cholesterol (compared to 30% with DSC), and lowering cholesterol levels to 11.1 mmol/L in 6 weeks. DF removed both LDL and LP-X from plasma, whereas DSC selectively decreased the LDL content. The reduction of plasma cholesterol levels was associated with a complete regression of the xanthomas, supporting DF apheresis as a first-choice treatment for patients with massive LP-X accumulation due to cholestasis., Liver disease may be complicated by changes in the patterns of blood lipids and lipoproteins. Cholestasis, the cessation of bile excretion, is associated with elevated free cholesterol and phospholipids and the production of an abnormal lipoprotein, lipoprotein-X (LP-X). LP-X consists of a two layer membrane compartment containing phospholipids, cholesterol, and small amounts of the protein albumin and other apolipoproteins. LP-X has a similar density as low-density-lipoprotein (LDL), lacks apolipoprotein B, and does not interact with the membrane site that specifically binds LDL. Hence, LP-X cannot transport cholesterol to the liver or regulate the production of cholesterol. Consequently, LP-X causes the accumulation of cholesterol and triglycerides in patients with cholestasis. This may be associated with the development of xanthomas, which are flat, slightly elevated, soft rounded patches or node-like skin lesions, and worsening of blood vessel disease. The elevated LP-X levels and development of xanthomas associated with cholestasis can be reduced by plasmapheresis, a procedure in which cellular elements of the blood are separated, and by other methods of plasma exchange. A case is described of a patient with severe cholestasis with increased cholesterol levels due to accumulation of LP-X and widespread formation of xanthomas. The patient was treated by LDL-apheresis, a procedure in which blood is removed from the body, and processed to reduce LDL levels. The double filtration (DF) technique of LDL-apheresis was more effective than the dextran-sulfate-cellulose (DSC) method in reducing total cholesterol. DF reduced both LDL and LP-X, whereas DSC reduced only LDL. A decrease in blood cholesterol levels was associated with complete regression of xanthomas. Thus, DF apheresis is beneficial for treating patients with accumulation of LP-X associated with cholestasis. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1991

39. Myocardial overexpression of ANKRD1 causes sinus venosus defects and progressive diastolic dysfunction.

Author

Piroddi, Nicoletta, Pesce, Paola, Scellini, Beatrice, Manzini, Stefano, Ganzetti, Giulia S, Badi, Ileana, Menegollo, Michela, Cora, Virginia, Tiso, Simone, Cinquetti, Raffaella, Monti, Laura, Chiesa, Giulia, Bleyl, Steven B, Busnelli, Marco, Dellera, Federica, Bruno, Daniele, Caicci, Federico, Grimaldi, Annalisa, Taramelli, Roberto, and Manni, Lucia

Abstract

Aims Increased Ankyrin Repeat Domain 1 (ANKRD1) levels linked to gain of function mutations have been associated to total anomalous pulmonary venous return and adult cardiomyopathy occurrence in humans. The link between increased ANKRD1 level and cardiac structural and functional disease is not understood. To get insight into this problem, we have generated a gain of function ANKRD1 mouse model by overexpressing ANKRD1 in the myocardium. Methods and results Ankrd1 is expressed non-homogeneously in the embryonic myocardium, with a dynamic nucleo-sarcomeric localization in developing cardiomyocytes. ANKRD1 transgenic mice present sinus venosus defect, which originates during development by impaired remodelling of early embryonic heart. Adult transgenic hearts develop diastolic dysfunction with preserved ejection fraction, which progressively evolves into heart failure, as shown histologically and haemodynamically. Transgenic cardiomyocyte structure, sarcomeric assembly, and stability are progressively impaired from embryonic to adult life. Postnatal transgenic myofibrils also present characteristic functional alterations: impaired compliance at neonatal stage and impaired lusitropism in adult hearts. Altogether, our combined analyses suggest that impaired embryonic remodelling and adult heart dysfunction in ANKRD1 transgenic mice present a common ground of initial cardiomyocyte defects, which are exacerbated postnatally. Molecular analysis showed transient activation of GATA4-Nkx2.5 transcription in early transgenic embryos and subsequent dynamic transcriptional modulation within titin gene. Conclusions ANKRD1 is a fine mediator of cardiomyocyte response to haemodynamic load in the developing and adult heart. Increased ANKRD1 levels are sufficient to initiate an altered cellular phenotype, which is progressively exacerbated into a pathological organ response by the high ventricular workload during postnatal life. Our study defines for the first time a unifying picture for ANKRD1 role in heart development and disease and provides the first mechanistic link between ANKRD1 overexpression and cardiac disease onset. [ABSTRACT FROM AUTHOR]

Published
2020
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40. Fenretinide treatment accelerates atherosclerosis development in apoE-deficient mice in spite of beneficial metabolic effects.

Author

Busnelli, Marco, Manzini, Stefano, Bonacina, Fabrizia, Soldati, Sabina, Barbieri, Silvia Stella, Amadio, Patrizia, Sandrini, Leonardo, Arnaboldi, Francesca, Donetti, Elena, Laaksonen, Reijo, Paltrinieri, Saverio, Scanziani, Eugenio, and Chiesa, Giulia

Subjects
THORACIC aorta, SINUS of valsalva, BODY composition, ABDOMINAL aorta, BLOOD lipids, WESTERN diet, LIPID metabolism, ENERGY metabolism, RETINOIDS, BIOLOGICAL models, DISEASE progression, RESEARCH, AORTIC diseases, LIVER, ANIMAL experimentation, RESEARCH methodology, ANTINEOPLASTIC agents, BLOOD sugar, MEDICAL cooperation, EVALUATION research, ATHEROSCLEROSIS, COMPARATIVE studies, WEIGHT loss, RESEARCH funding, AORTA, SPLEEN, LIPIDS, MICE
Abstract

Background and Purpose: Fenretinide, a synthetic retinoid derivative first investigated for cancer prevention and treatment, has been shown to ameliorate glucose tolerance, improve plasma lipid profile and reduce body fat mass. These effects, together with its ability to inhibit ceramide synthesis, suggest that fenretinide may have an anti-atherosclerotic action.Experimental Approach: To this aim, nine-week-old apoE-knockout (EKO) female mice were fed for twelve weeks a Western diet, without (control) or with (0.1% w/w) fenretinide. As a reference, wild-type (WT) mice were treated similarly. Growth and metabolic parameters were monitored throughout the study. Atherosclerosis development was evaluated in the aorta and at the aortic sinus. Blood and lymphoid organs were further characterized with thorough cytological/histological and immunocytofluorimetric analyses.Key Results: Fenretinide treatment significantly lowered body weight, glucose levels and plasma levels of total cholesterol, triglycerides, and phospholipids. In the liver, fenretinide remarkably reduced hepatic glycogenosis and steatosis driven by the Western diet. Treated spleens were abnormally enlarged, with severe follicular atrophy and massive extramedullary haematopoiesis. Severe renal hemosiderin deposition was observed in treated EKO mice. Treatment resulted in a threefold increase of total leukocytes (WT and EKO) and raised the activated/resting monocyte ratio in EKO mice. Finally, atherosclerosis development was markedly increased at the aortic arch, thoracic and abdominal aorta of fenretinide-treated mice.Conclusions and Implications: We provide the first evidence that, despite beneficial metabolic effects, fenretinide treatment may enhance the development of atherosclerosis. [ABSTRACT FROM AUTHOR]

Published
2020
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44. Atherogenesis in transgenic mice expressing human apolipoprotein(a)

Author

Lawn, Richard M., Wade, David P., Hammer, Robert E., Chiesa, Giulia, Verstuyft, Judy G., and Rubin, Edward M.

Subjects
Atherosclerosis -- Development and progression, Genetically modified mice -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

The risk factors for atherosclerosis are well known, but with one exception its causes remain unclear. A study using transgenic mice that express human apolipoprotein(a) may help clarify matters. Experimental mice exposed to a high fat diet develop more lipid-staining lesions in the aorta than non-transgenic mice on a similar diet or transgenic mice on a normal diet. Apolipoprotein(a) was found to localize with lipids in lesion areas suggesting that the observed differences in atherogenesis results from the protein.

Published
1992

45. Integrated high-throughput mirnomics and lipidomics allow a detailed dissection of mirna to molecular lipid levels correlations in wild-type, PCSK9 and LDLR knockout mice

Author

Manzini, Stefano, primary, Busnelli, Marco, additional, Hilvo, Mika, additional, Chiara, Matteo, additional, Parolini, Cinzia, additional, Dellera, Federica, additional, Ganzetti, Giulia, additional, Horner, David, additional, Laaksonen, Reijo, additional, and Chiesa, Giulia, additional

Published
2017
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47. Dysregulated expression of Ankyrin repeat domain 1 in the developing myocardium causes anomalous venous return and morphogenetic defects by impairing cardiac remodelling

Author

Parolini, Cinzia, primary, Ganzetti, Giulia Sara, additional, Manzini, Stefano, additional, Monti, Laura, additional, Chiesa, Giulia, additional, Busnelli, Marco, additional, Dellera, Federica, additional, Badi, Ileana, additional, Campione, Marina, additional, and Acquati, Francesco, additional

Published
2017
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49. Liver-specific deletion of the Plpp3 gene alters plasma lipid composition and worsens atherosclerosis in apoE−/− mice

Author

Busnelli, Marco, primary, Manzini, Stefano, additional, Hilvo, Mika, additional, Parolini, Cinzia, additional, Ganzetti, Giulia S., additional, Dellera, Federica, additional, Ekroos, Kim, additional, Jänis, Minna, additional, Escalante-Alcalde, Diana, additional, Sirtori, Cesare R., additional, Laaksonen, Reijo, additional, and Chiesa, Giulia, additional

Published
2017
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50. Skin morphology in double apoA-I/apoE knock-out mice: a structural and ultrastructural study

Author

Arnaboldi, Francesca, Busnelli, Marco, Parolini, Cinzia, Manzini, Stefano, Ganzetti, Giulia S., Dellera, Federica, and Chiesa, Giulia

Subjects
lipids (amino acids, peptides, and proteins), Apolipoproteins, ApoE-KO, cholesterol clefts, HDLs, skin morphology
Abstract

Apolipoprotein(apo)A-I, the main protein component of high density lipoproteins (HDLs), plays a major role in cholesterol removal from peripheral tissues and increasing evidence supports its function as an important regulator of the immune response (Annema et al., 2013). The aim of the study was to evaluate the effect of apoA-I deficiency in dyslipidemic mice, when fed a low-fat/low-cholesterol diet. Three lines of male mice were considered: wild-type mice as controls, apoE-KO mice as dyslipidemic model (Zhang et al.,1992) and apoA-I/apoE double KO mice (DKO mice). Whereas in wild-type mice cholesterol circulates almost exclusively in HDLs, apoE-KO mice are hypercholesterolemic and cholesterol mostly circulates in low-density lipoproteins. In DKO mice, cholesterol levels are comparable to wild-type mice, but HDLs are almost absent and cholesterol entirely accumulates in low-density lipoproteins. In the present study, all animals were maintained on a low-fat/low-cholesterol diet up to 30 weeks of age. At sacrifice, skin biopsies from two different anatomical areas (thoracic and abdominal regions) were harvested from each animal and processed for both light (LM) and transmission electron microscopy (TEM). Whereas the skin of apoE-KO mice was comparable to that of control mice, LM analysis in DKO mice revealed an increase in dermal thickness and a massive presence of foam cells and lymphocytes. TEM analysis showed the presence of cholesterol clefts in the papillary dermis and inside foam cells in the reticular dermis. In conclusion, our results demonstrate that in DKO mice fed a low-fat/low-cholesterol diet, the lack of apoA-I is responsible for an aberrant skin morphology, with an exacerbated inflammatory response, possibly caused by a local cholesterol accumulation., Italian Journal of Anatomy and Embryology, Vol 119, No 1 (Supplement) 2014

Published
2015
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