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2. Contributors

Author

Agrawala, Paban K., primary, Alvarado, Christopher, additional, Amir, Mohammed, additional, Bernau, Ksenija, additional, Bhattacharya, Aditi, additional, Biswas, Biswajit, additional, Block, Megan, additional, Boosani, Anvitha, additional, Boosani, Chandra S., additional, Brasier, Allan R., additional, Brown, Julia A., additional, Chakraborty, Rajasree, additional, Das, Abhijit, additional, Dasari, Nikhitha, additional, DiStefano, Johanna K., additional, Dwarakanath, B.S., additional, Fukai, Tohru, additional, Gaikwad, Anil Bhanudas, additional, Gong, Fangyan, additional, Gornati, Rosalba, additional, Goswami, Ritobrata, additional, Gunasekar, Palanikumar, additional, Gupta, Noopur, additional, Hassan, Ebrahim Bani, additional, Jadhav, Gopal P., additional, Jain, Natasha Victoria, additional, Jiang, Fang, additional, Jiang, Wanlin, additional, Kreger, Jonathan, additional, Kulkarni, Yogesh A., additional, Le, Patricia N., additional, Liu, Lei, additional, Maini, Jayant, additional, Mondal, Papiya, additional, Nakai, Kenta, additional, Natarajan, Umamaheswari, additional, Olson, Michael T., additional, Pagiatakis, Christina, additional, Pandkar, Madhura R., additional, Pant, Amit M., additional, Papait, Roberto, additional, Patnaik, Srinivas, additional, Pelham, Christopher J., additional, Prakash, Anu, additional, Rathinavelu, Appu, additional, Sandbo, Nathan, additional, Sarkar, Subhajit, additional, Sharma, Ajay, additional, Sharma, Nisha, additional, Sharma, Vineeta, additional, Shiva, Niharika, additional, Shukla, Sanjeev, additional, Singh, Lakshman, additional, Singh, Sukhveer, additional, Singhal, Saurabh, additional, Srivastava, Vikas, additional, Sudhahar, Varadarajan, additional, Tiffon, Céline, additional, Ushio-Fukai, Masuko, additional, Vandenbon, Alexis, additional, Weng, Judy, additional, Woo, Jesse, additional, Wu, Xiumei, additional, Yadav, Pooja, additional, and Zeng, Melody Y., additional

Published
2023
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7. Cardiac Aging Is Promoted by Pseudohypoxia Increasing p300-Induced Glycolysis

Author

Serio, Simone, primary, Pagiatakis, Christina, additional, Musolino, Elettra, additional, Felicetta, Arianna, additional, Carullo, Pierluigi, additional, Laura Frances, Javier, additional, Papa, Laura, additional, Rozzi, Giacomo, additional, Salvarani, Nicolò, additional, Miragoli, Michele, additional, Gornati, Rosalba, additional, Bernardini, Giovanni, additional, Condorelli, Gianluigi, additional, and Papait, Roberto, additional

Published
2023
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12. Contributors

Author

Ait-Si-Ali, Slimane, primary, Albini, Sonia, additional, Atzmon, Gil, additional, Badylak, Stephen F., additional, Barnstable, C.J., additional, Biferali, Beatrice, additional, Caporale, Nicolò, additional, Chen, Zhaoyi, additional, Chiacchiera, Fulvio, additional, Coffman, James A., additional, D’Angelo, William, additional, Dean, Wendy, additional, Eriksson, Jonas, additional, Fernández, Agustín F., additional, Fraga, Mario F., additional, Guil, Sònia, additional, Gutman, Danielle, additional, Hadi, Nur Annies Abd, additional, Hanna, Courtney W., additional, Josipović, Nataša, additional, Julian, Lisa M., additional, Mai, Antonello, additional, Marelli, Luca, additional, McCarthy, Ryan L., additional, McLaughlin, Katy A., additional, Meehan, Richard R., additional, Mozzetta, Chiara, additional, Nicetto, Dario, additional, Oliveira-Mateos, Cristina, additional, Ottaviano, Raffaele, additional, Pagiatakis, Christina, additional, Palacios, Daniela, additional, Papait, Roberto, additional, Papantonis, Argyris, additional, Pennings, Sari, additional, Pérez, Raúl F., additional, Petchreing, Petchroi, additional, Pietrobon, Adam, additional, Popova, E.Y., additional, Revuelta, Ailsa, additional, Sánchez-Castillo, Anaís, additional, Santamarina, Pablo, additional, Serio, Simone, additional, Stanford, William L., additional, Stazi, Giulia, additional, Testa, Giuseppe, additional, Valente, Sergio, additional, Viscomi, Maria Teresa, additional, Zakharova, Vlada, additional, Zaret, Kenneth S., additional, and Zwergel, Clemens, additional

Published
2019
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14. Single-Cell Sequencing of Mouse Heart Immune Infiltrate in Pressure Overload–Driven Heart Failure Reveals Extent of Immune Activation

Author

Martini, Elisa, Kunderfranco, Paolo, Peano, Clelia, Carullo, Pierluigi, Cremonesi, Marco, Schorn, Tilo, Carriero, Roberta, Termanini, Alberto, Colombo, Federico Simone, Jachetti, Elena, Panico, Cristina, Faggian, Giuseppe, Fumero, Andrea, Torracca, Lucia, Molgora, Martina, Cibella, Javier, Pagiatakis, Christina, Brummelman, Jolanda, Alvisi, Giorgia, Mazza, Emilia Maria Cristina, Colombo, Mario Paolo, Lugli, Enrico, Condorelli, Gianluigi, and Kallikourdis, Marinos

Published
2019
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16. Iron oxide nanoparticles with and without cobalt functionalization provoke changes in the transcription profile via epigenetic modulation of enhancer activity

Author

European Commission, Ministero dell'Istruzione, dell'Università e della Ricerca, Gamberoni, Federica, Borgese, Marina, Pagiatakis, Christina, Armenia, Ilaria, Grazú, Valeria, Gornati, Rosalba, Serio, Simone, Papait, Roberto, Bernardini, Giovanni, European Commission, Ministero dell'Istruzione, dell'Università e della Ricerca, Gamberoni, Federica, Borgese, Marina, Pagiatakis, Christina, Armenia, Ilaria, Grazú, Valeria, Gornati, Rosalba, Serio, Simone, Papait, Roberto, and Bernardini, Giovanni

Abstract

Despite the progress in the field of nanotoxicology, much about the cellular mechanisms that mediate the adverse effects of nanoparticles (NPs) and, in particular, the possible role of epigenetics in nanotoxicity, remains to be clarified. Therefore, we studied the changes occurring in the genome-wide distribution of H3K27ac, H3K4me1, H3K9me2, and H3K27me3 histone modifications and compared them with the transcriptome after exposing NIH3T3 cells to iron-based magnetic NPs (i.e., Fe2O3 and Fe2O3@Co NPs). We found that the transcription response is mainly due to changes in the genomic distribution of H3K27ac that can modulate the activity of enhancers. We propose that alteration of the epigenetic landscape is a key mechanism in defining the gene expression program changes resulting in nanotoxicity. With this approach, it is possible to construct a data set of genomic regions that could be useful for defining toxicity in a manner that is more comprehensive than what is possible with the present toxicology assays.

Published
2023

21. Contributors

Author

Araki, Yasuto, Beristain-Pozos, Juan Daniel, Bhadra, Mridula, Bhebhe, Arnold, Bisht, Deepa, Burton, Mark, Castro-Morales, Diana, Chen, Pao-Yang, Climent, Montserrat, Colón-Caraballo, Mariano, Coppedè, Fabio, Cozma, Angela, Davey, Matthew G., Dugué, Pierre-Antoine, Edwards, Dean P., El-Awady, Raafat, El-Heis, Sarah, Elia, Leonardo, Eriksson, Johan G., Farina, Floriana Maria, Flores-Caldera, Idhaliz, Fodor, Adriana, Fuso, Andrea, Godfrey, Keith M., Gomez-Verjan, Juan Carlos, Grill, Jacques, Gupta, Manish Kumar, Hall, Ignacio Fernando, Hedrich, Christian Michael, Hopper, John L., Hoyo, Cathrine, Huang, Shixia, Huang, Yu-Chun, Karmaus, Wilfried, Katsardis, Charis, Kong, Dewei, Kowluru, Anjaneyulu, Kowluru, Renu A., Li, Shuai, Lillycrop, Karen A., Lim, Lillian Yuxian, Lin, Guan-Jun, Lin, Pei-Yu, Løkhammer, Solveig, Lyra Sheu, Chiao-Yu, Mahnke, Amanda H., Mastrototaro, Giuseppina, McConkey, Haley, Meyering, Shabana S., Miller, Nicola, Milne, Roger L., Mimura, Toshihide, Minarovits, Janos, Miranda, Rajesh C., Mohan, Vasavi, Mohiuddin, Mohammed Khaliq, Mukherjee, Nandini, Mutirangura, Apiwat, Niller, Hans Helmut, Pagiatakis, Christina, Papamichael, Maria Michelle, Park, Sarah S., Perales, Selene G., Pruksananonda, Kamthorn, Rajasingh, Johnson, Rajasingh, Sheeja, Ramadan, Wafaa S.H., Rivero-Segura, Nadia Alejandra, Roman, Gabriela, Rouleau, Etienne, Rousseau, Léa Guerrini, Rouzer, Siara K., Rusu, Adriana, Saber-Ayad, Maha M., Sachan, Manisha, Sadikovic, Bekim, Saldanha, Sabita N., Salem, Nihal A., Sandoval-Rodríguez, Francisco Ernesto, Sassi, Hela, Seow, Wei Qiang, Sessa, Alessandro, Sharma, Nikita, Shi, Zhongcheng, Sitar-Taut, Adela, Skaar, David, Suharoschi, Ramona, Teo, Adrian Kee Keong, Thumoju, Sravya, Tint, Mya Thway, Tollefsbol, Trygve O., Tseng, Alexander M., Vulturar, Romana, Wang, Xuan, Wasinarom, Artisa, Watson, Erica D., Young, Nicolas L., Zhou, Zhigang, Zaghi, Mattia, and Ziyab, Ali H.

Published
2024
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23. Myocardial hypoxic stress mediates functional cardiac extracellular vesicle release

Author

Anselmo, Achille, primary, Frank, Derk, additional, Papa, Laura, additional, Viviani Anselmi, Chiara, additional, Di Pasquale, Elisa, additional, Mazzola, Marta, additional, Panico, Cristina, additional, Clemente, Francesca, additional, Soldani, Cristiana, additional, Pagiatakis, Christina, additional, Hinkel, Rabea, additional, Thalmann, Ruth, additional, Kozlik-Feldmann, Reiner, additional, Miragoli, Michele, additional, Carullo, Pierluigi, additional, Vacchiano, Marco, additional, Chaves-Sanjuan, Antonio, additional, Santo, Nadia, additional, Losi, Maria Angela, additional, Ferrari, Matteo Carlo, additional, Puca, Annibale Alessandro, additional, Christiansen, Vincent, additional, Seoudy, Hatim, additional, Freitag-Wolf, Sandra, additional, Frey, Norbert, additional, Dempfle, Astrid, additional, Mercola, Mark, additional, Esposito, Giovanni, additional, Briguori, Carlo, additional, Kupatt, Christian, additional, and Condorelli, Gianluigi, additional

Published
2021
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27. Using Epigenetics as a Pharmacological Tool in Heart Regeneration

Author

Serio Simone, Roberto Papait, and Pagiatakis Christina

Subjects
DNA methylation, Heart development, Mechanism (biology), business.industry, Regeneration (biology), non-coding RNA, Heart failure, heart development, DNA methylation, Histone acetylation, histone methylation, non-coding RNA, cardiac trans-differentiation, induced pluripotent stem cells (iPSs), Heart failure, heart development, Bioinformatics, medicine.disease, cardiac trans-differentiation, Histone acetylation, medicine, Gene silencing, Epigenetics, histone methylation, induced pluripotent stem cells (iPSs), business, Reprogramming
Abstract

Heart failure (HF) is the ultimate outcome of many cardiovascular pathologies and the leading cause of morbidity and mortality worldwide. An exciting therapeutic strategy for HF is cardiac regeneration, the feasibility of which is supported by the ability of the neonatal heart to regenerate following cardiac injury. However, the major limitation facing the application of this strategy is the inability of adult cardiomyocytes to proliferate. This is a consequence of the gene expression program underlying cardiomyocyte differentiation that promotes silencing of proliferative genes. One mechanism that plays a key role in defining this gene expression program is epigenetics. Recent reports have shown that epigenetic mechanisms similar to those that govern gene expression in heart development govern the gene expression changes occurring in HF. This chapter provides an overview of the epigenetic mechanisms involved in cardiac development and disease and how they can influence cardiac reprogramming and regeneration.

Published
2019

30. Late Breaking Science posters657Aldehyde Dehydrogenase2 regulates senescence in the vascular endothelium658Monoamine oxidase is over-activated in the left and right ventricles from human ischemic hearts: an intriguing therapeutic target659A novel assay for regulating transcription factors by flow660Remote ischaemic conditioning reduces infarct size in animal in vivo models of ischaemia-reperfusion injury: a systematic review and meta-analysis661The Role of Histone Methyl-transferase G9a in Heart Homeostasis and Cardiac Hypertrophy: a Potential Therapeutic Target for Heart Failure663The extracellular matrix SPARCs cardiac contraction during health and disease664A proteomic investigation into the mechanisms of VEGF-adhesion receptor crosstalk in endothelial cells665Assessing the role of PMCA1 in arrhythmia development relating to β-adrenergic signalling667The expression of beta myosin isoform MYH7B correlates with severity of left ventricular systolic dysfunction in patients with hypertrophic cardiomyopathy668Spatial heterogeneity of sympathetic response in the rabbit myocardium

Author

Donnini, Sandra, primary, Miceli, Caterina, primary, Krams, R.M., primary, Bromage, Daniel, primary, Papait, Roberto, primary, Johnson, Daniel, primary, James, Jenny, primary, Wilson, Claire, primary, Sartorio, Carmem Luiza, primary, Anderson, SE., primary, Terzuoli, Erika, additional, Finetti, Federica, additional, Ziche, Marina, additional, Rigacci, Stefania, additional, Bargelli, Valentina, additional, Giordano, Carla, additional, Raimondi, Laura, additional, Nediani, Chiara, additional, Miceli, Caterina, additional, Pedrigi, R.M., additional, Kis, Z., additional, Pickard, Jack, additional, Rossello, Xavier, additional, Burke, Niall, additional, Ziff, Oliver, additional, Yellon, Derek, additional, Davidson, Sean, additional, Pagiatakis, Christina, additional, Rusconi, Francesca, additional, Carullo, Pierluigi, additional, Serio, Simone, additional, Condorelli, Gianluigi, additional, Deckx, S, additional, Rienks, M., additional, Carai, P., additional, Van Deel, E., additional, Van Der Velden, J., additional, Sipido, K.R., additional, Heymans, S, additional, Papageorgiou, A., additional, Humphries, Jonathan, additional, Canfield, Ann, additional, Humphries, Martin, additional, Bertoli, Gloria, additional, Lazzeroni, Davide, additional, Rimoldi, Ornella, additional, Esposito, Alessandra, additional, Peretto, Giovanni, additional, Damascelli, Anna, additional, De Cobelli, Francesco, additional, Alfieri, Ottavio, additional, Camici, Paolo Guido, additional, Smith, GL., additional, and Myles, RC., additional

Published
2016
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32. TGFβ- TAZ/ SRF signalling regulates vascular smooth muscle cell differentiation.

Author

Pagiatakis, Christina, Sun, Dandan, Tobin, Stephanie W., Miyake, Tetsuaki, and McDermott, John C.

Subjects
*TRANSFORMING growth factors, *CELLULAR signal transduction, *VASCULAR smooth muscle, *TRANSCRIPTION factors, *SMALL interfering RNA
Abstract

Vascular smooth muscle cells ( VSMCs) do not terminally differentiate; they modulate their phenotype between proliferative and differentiated states, which is a major factor contributing to vascular diseases. TGFβ signalling has been implicated in inducing VSMC differentiation, although the exact mechanism remains largely unknown. Our goal was to assess the network of transcription factors involved in the induction of VSMC differentiation, and to determine the role of TAZ in promoting the quiescent VSMC phenotype. TGFβ robustly induces VSMC marker genes in 10T1/2 mouse embryonic fibroblast cells and the potent transcriptional regulator TAZ has been shown to retain Smad complexes on DNA. Thus, the role of TAZ in regulation of VSMC differentiation was studied. Using primary aortic VSMCs coupled with si RNA-mediated gene silencing, our studies reveal that TAZ is required for TGFβ induction of smooth muscle genes and is also required for the differentiated VSMC phenotype; synergy between TAZ and SRF, and TAZ and Myocardin (MyoC856), in regulating smooth muscle gene activation was observed. These data provide evidence of components of a novel signalling pathway that links TGFβ signalling to induction of smooth muscle genes through a mechanism involving regulation of TAZ and SRF proteins. In addition, we report a physical interaction of TAZ and MyoC856. These observations elucidate a novel level of control of VSMC induction which may have implications for vascular diseases and congenital vascular malformations. [ABSTRACT FROM AUTHOR]

Published
2017
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34. Protein Kinase A-regulated Assembly of a MEF2·HDAC4 Repressor Complex Controls c-Jun Expression in Vascular Smooth Muscle Cells

Author

Gordon, Joseph W., primary, Pagiatakis, Christina, additional, Salma, Jahan, additional, Du, Min, additional, Andreucci, John J., additional, Zhao, Jianzhong, additional, Hou, Guangpei, additional, Perry, Robert L., additional, Dan, Qinghong, additional, Courtman, David, additional, Bendeck, Michelle P., additional, and McDermott, John C., additional

Published
2009
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35. Protein kinase A-regulated assembly of a MEF2{middle dot}HDAC4 repressor complex controls c-Jun expression in vascular smooth muscle cells.

Author

Gordon JW, Pagiatakis C, Salma J, Du M, Andreucci JJ, Zhao J, Hou G, Perry RL, Dan Q, Courtman D, Bendeck MP, and McDermott JC

Subjects
Animals, Cell Nucleus metabolism, MEF2 Transcription Factors, Mice, Models, Biological, Muscle, Smooth, Vascular metabolism, Nuclear Proteins metabolism, Promoter Regions, Genetic, RNA Interference, RNA, Small Interfering metabolism, Rats, Trans-Activators metabolism, Cyclic AMP-Dependent Protein Kinases metabolism, Gene Expression Regulation, Histone Deacetylases metabolism, Myogenic Regulatory Factors metabolism, Proto-Oncogene Proteins c-jun metabolism
Abstract

Vascular smooth muscle cells (VSMCs) maintain the ability to modulate their phenotype in response to changing environmental stimuli. This phenotype modulation plays a critical role in the development of most vascular disease states. In these studies, stimulation of cultured vascular smooth muscle cells with platelet-derived growth factor resulted in marked induction of c-jun expression, which was attenuated by protein kinase Cdelta and calcium/calmodulin-dependent protein kinase inhibition. Given that these signaling pathways have been shown to relieve the repressive effects of class II histone deacetylases (HDACs) on myocyte enhancer factor (MEF) 2 proteins, we ectopically expressed HDAC4 and observed repression of c-jun expression. Congruently, suppression of HDAC4 by RNA interference resulted in enhanced c-jun expression. Consistent with these findings, mutation of the MEF2 cis-element in the c-jun promoter resulted in promoter activation during quiescent conditions, suggesting that the MEF2 cis-element functions as a repressor in this context. Furthermore, we demonstrate that protein kinase A attenuates c-Jun expression by promoting the formation of a MEF2.HDAC4 repressor complex by inhibiting salt-inducible kinase 1. Finally, we document a physical interaction between c-Jun and myocardin, and we document that forced expression of c-Jun represses the ability of myocardin to activate smooth muscle gene expression. Thus, MEF2 and HDAC4 act to repress c-Jun expression in quiescent VSMCs, protein kinase A enhances this repression, and platelet-derived growth factor derepresses c-Jun expression through calcium/calmodulin-dependent protein kinases and novel protein kinase Cs. Regulation of this molecular "switch" on the c-jun promoter may thus prove critical for toggling between the activated and quiescent VSMC phenotypes.

Published
2009
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