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ChenJinghai

2019-09-03   |  

Name: ChenJinghai
Post: Professor
Position: Principle Investigator
Education: Ph.D.
Professional: Biochemistry and Molecular Biology
Departments: The Institute of Translational Medicine
Research: Cardiac Disease and Regeneration
TEL: 0571-86971930
E-mail: jinghaichen@zju.edu.cn
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Profile

Education:09/2001-12/2006  PhD,    Peking Union Medical College & Chinese Academy of Medical Science09/1997-07/2001  BS,    Zhejiang UniversityAcademic Appointments03/2015- Professor,    Institute of Translational Medicine of Zhejiang University, The Second Affiliated Hospital of Zhejiang University, Hangzhou, Zhejiang, China.12/2011-03/2015 Instructor,    Harvard Medical School, Boston Children’s Hospital, Boston, MA, USA02/2010-12/2011 Postdoctoral Fellow,    Harvard Medical School, Boston Children’s Hospital, Boston, MA, USA03/2007-02/2010 Postdoctoral Fellow,    Sanford Research, University of South Dakota, Sioux Falls, SD, USAResearch AreaCardiovascular diseases are the main cause of death worldwide. The adult heart is primarily composed of terminally differentiated cardiomyocytes that exit the cell cycle. Under disease stress, cardiomyocytes die and the survival cardiomyocytes compensatorily turn into hypertrophic remodeling. Then heart gets decompensation, eventually leading to heart failure. The molecular mechanism that controls cardiac remodeling and regeneration during diseases are not fully understood. My researches have been focused on cardiovascular diseases from development, adult heart remodeling and cardiac regeneration. Especially, I would like, but not limited, to elucidate how noncoding RNA regulates cardiac hypertrophy and cardiac regeneration during the cardiovascular diseases. We use cardiac cell system, mouse genetic model and AAV system to study the cardiovascular diseases. We apply a variety of molecular, cellular, and genetic approaches.Selected Publications (1) Ding J, Chen J, Wang Y, Kataoka M, Ma L, Zhou P, Hu X, Lin Z, Nie M, Deng ZL, Pu WT, Wang DZ. Trbp regulates heart function through microRNA-mediated Sox6 repression. Nature Genetics. 2015 ;47(7):776-83.(2) Seok H#, Chen J#, Kataoka M, Huang ZP, Ding J, Yan J, Hu X, Wang DZ. Loss of MicroRNA-155 protects the heart from pathological cardiac hypertrophy. Circulation Research. 2014;114 (10):1585-95. (# co-first) (3) Chen J, Huang ZP, Seok H, Ding J, Kataoka M, Zhang Z, Hu X, Wang G, Lin Z, Wang S, Pu W, Liao R, Wang DZ. mir-17-92 Cluster is Required for and Sufficient to Induce Cardiomyocyte Proliferation in Postnatal and Adult Hearts. Circulation Research. 2013; 112(12):1557-66. (4) Huang ZP#, Chen J#, Seok H, Zhang Z, Kataoka M, Hu X, Wang DZ. MicroRNA-22 Regulates Cardiac Hypertrophy and Remodeling in Response to Stress. Circulation Research. 2013 112(9):1234-43. (# Co-first) (5) Chen J, Wang DZ. microRNAs in cardiovascular development. Journal of Molecular and Cellular Cardiology. 2012;52(5):949-57. (6) Chen J, Ortmeier SB, Savinova OV, Nareddy VB, Beyer AJ, Wang D, Gerdes AM. Thyroid hormone induces sprouting angiogenesis in adult heart of hypothyroid mice through the PDGF-Akt pathway. Journal of Cellular and Molecular Medicine. 2012 16(11):2726-35. (7) Chen J, Shearer GC, Chen Q, Healy CL, Beyer AJ, Nareddy VB, Gerdes AM, Harris WS, O'Connell TD, Wang D. Omega-3 Fatty Acids Prevent Pressure Overload-Induced Cardiac Fibrosis Through Activation of Cyclic GMP/Protein Kinase G Signaling in Cardiac Fibroblasts. Circulation. 2011;123(6):584-93.  (8) Chen J, Baydoun AR, Xu R, Deng L, Zhu W, Cong X, Hu S, ChenX. Lysophosphatidic Acid Protects Mesenchymal Stem Cells against Hypoxia and Serum Deprivation-Induced Apoptosis. Stem Cells. 2008;26(1):135-45. (9) Chen J, Chen Y, Zhu W, Han Y, Han B, Xu R, Deng L, Cai Y, Cong X, Yang Y, Hu S, Chen X.  Specific LPA receptor subtype mediation of LPA-induced hypertrophy of cardiac myocytes and involvement of Akt and NFkappaB signal pathways. Journal of Cellular Biochemistry. 2008;103(6):1718-31. (10) Chen J, Han Y, Zhu W, Ma R, Han B, Cong X, Hu S, Chen X. Specific receptor subtype mediation of LPA-induced dual effects in cardiac fibroblasts. FEBS Letters. 2006;580(19):4737-45.