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6 results on '"Gu, Mingxia"'

2. Epigenetic Regulation of Phosphodiesterases 2A and 3A Underlies Compromised β-Adrenergic Signaling in an iPSC Model of Dilated Cardiomyopathy

Author

Wu, Haodi, Lee, Jaecheol, Vincent, Ludovic G, Wang, Qingtong, Gu, Mingxia, Lan, Feng, Churko, Jared M, Sallam, Karim I, Matsa, Elena, Sharma, Arun, Gold, Joseph D, Engler, Adam J, Xiang, Yang K, Bers, Donald M, and Wu, Joseph C

Subjects
Medical Physiology, Biomedical and Clinical Sciences, Stem Cell Research, Rare Diseases, Stem Cell Research - Induced Pluripotent Stem Cell - Human, Clinical Research, Genetics, Cardiovascular, Stem Cell Research - Induced Pluripotent Stem Cell, Heart Disease, 2.1 Biological and endogenous factors, Aetiology, Adrenergic beta-Agonists, Cardiomyopathy, Dilated, Cell Differentiation, Cells, Cultured, Cyclic Nucleotide Phosphodiesterases, Type 2, Cyclic Nucleotide Phosphodiesterases, Type 3, Epigenesis, Genetic, Heart Rate, Humans, Induced Pluripotent Stem Cells, Isoproterenol, Models, Cardiovascular, Mutant Proteins, Mutation, Myocardial Contraction, Myocytes, Cardiac, Receptors, Adrenergic, beta, Signal Transduction, Troponin T, Up-Regulation, Biological Sciences, Medical and Health Sciences, Developmental Biology, Biological sciences, Biomedical and clinical sciences
Abstract

β-adrenergic signaling pathways mediate key aspects of cardiac function. Its dysregulation is associated with a range of cardiac diseases, including dilated cardiomyopathy (DCM). Previously, we established an iPSC model of familial DCM from patients with a mutation in TNNT2, a sarcomeric protein. Here, we found that the β-adrenergic agonist isoproterenol induced mature β-adrenergic signaling in iPSC-derived cardiomyocytes (iPSC-CMs) but that this pathway was blunted in DCM iPSC-CMs. Although expression levels of several β-adrenergic signaling components were unaltered between control and DCM iPSC-CMs, we found that phosphodiesterases (PDEs) 2A and PDE3A were upregulated in DCM iPSC-CMs and that PDE2A was also upregulated in DCM patient tissue. We further discovered increased nuclear localization of mutant TNNT2 and epigenetic modifications of PDE genes in both DCM iPSC-CMs and patient tissue. Notably, pharmacologic inhibition of PDE2A and PDE3A restored cAMP levels and ameliorated the impaired β-adrenergic signaling of DCM iPSC-CMs, suggesting therapeutic potential.

Published
2015

5. Intrinsic Endocardial Defects Contribute to Hypoplastic Left Heart Syndrome

Author

Miao, Yifei, primary, Tian, Lei, additional, Martin, Marcy, additional, Paige, Sharon L., additional, Galdos, Francisco X., additional, Li, Jibiao, additional, Klein, Alyssa, additional, Zhang, Hao, additional, Ma, Ning, additional, Wei, Yuning, additional, Stewart, Maria, additional, Lee, Soah, additional, Moonen, Jan-Renier, additional, Zhang, Bing, additional, Grossfeld, Paul, additional, Mital, Seema, additional, Chitayat, David, additional, Wu, Joseph C., additional, Rabinovitch, Marlene, additional, Nelson, Timothy J., additional, Nie, Shuyi, additional, Wu, Sean M., additional, and Gu, Mingxia, additional

Published
2020
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6. Patient-Specific iPSC-Derived Endothelial Cells Uncover Pathways that Protect against Pulmonary Hypertension in BMPR2 Mutation Carriers

Author

Gu, Mingxia, primary, Shao, Ning-Yi, additional, Sa, Silin, additional, Li, Dan, additional, Termglinchan, Vittavat, additional, Ameen, Mohamed, additional, Karakikes, Ioannis, additional, Sosa, Gustavo, additional, Grubert, Fabian, additional, Lee, Jaecheol, additional, Cao, Aiqin, additional, Taylor, Shalina, additional, Ma, Yu, additional, Zhao, Zhixin, additional, Chappell, James, additional, Hamid, Rizwan, additional, Austin, Eric D., additional, Gold, Joseph D., additional, Wu, Joseph C., additional, Snyder, Michael P., additional, and Rabinovitch, Marlene, additional

Published
2017
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