Myocyte-specific overexpressing HDAC4 promotes myocardial ischemia/reperfusion injury
文献类型：期刊论文
| 作者 | Wang, Hao2; Zhao, Yu2; Wang, Jianguo2; Zhao, Ting C.2; Zhang, Ling3; Dubielecka, Patrycja M.3; Zhuang, Shougang3; Qin, Gangjian4; Chin, Y. Eugene5; Kao, Race L.1 |
| 刊名 | MOLECULAR MEDICINE
 |
| 出版日期 | 2018 |
| 卷号 | 24期号:-页码:UNSP 37 |
| 关键词 | Histone deacetylase4 (HDAC4) Ischemia/reperfusion Myocardial function |
| ISSN号 | 1076-1551 |
| DOI | 10.1186/s10020-018-0037-2 |
| 文献子类 | Article |
| 英文摘要 | Background: Histone deacetylases (HDACs) play a critical role in modulating myocardial protection and cardiomyocyte survivals. However, Specific HDAC isoforms in mediating myocardial ischemia/reperfusion injury remain currently unknown. We used cardiomyocyte-specific overexpression of active HDAC4 to determine the functional role of activated HDAC4 in regulating myocardial ischemia and reperfusion in isovolumetric perfused hearts. Methods: In this study, we created myocyte-specific active HDAC4 transgenic mice to examine the functional role of active HDAC4 in mediating myocardial I/R injury. Ventricular function was determined in the isovolumetric heart, and infarct size was determined using tetrazolium chloride staining. Results: Myocyte-specific overexpressing activated HDAC4 in mice promoted myocardial I/R injury, as indicated by the increases in infarct size and reduction of ventricular functional recovery following I/R injury. Notably, active HDAC4 overexpression led to an increase in LC-3 and active caspase 3 and decrease in SOD-1 in myocardium. Delivery of chemical HDAC inhibitor attenuated the detrimental effects of active HDAC4 on I/R injury, revealing the pivotal role of active HDAC4 in response to myocardial I/R injury. Conclusions: Taken together, these findings are the first to define that activated HDAC4 as a crucial regulator for myocardial ischemia and reperfusion injury. |
| 学科主题 | Biochemistry & Molecular Biology ; Cell Biology ; Research & Experimental Medicine |
| WOS关键词 | HISTONE DEACETYLASE INHIBITION ; CARDIAC-HYPERTROPHY ; DEPENDENT PATHWAY ; HDA1P |
| 语种 | 英语 |
| WOS记录号 | WOS:000439183700001 |
| 出版者 | SPRINGER |
| 版本 | 出版稿 |
| 源URL | [http://202.127.25.144/handle/331004/683]  |
| 专题 | 中国科学院上海生命科学研究院营养科学研究所 |
| 作者单位 | 1.East Tennessee State Univ, Dept Surg, Johnson City, TN USA, 2.Boston Univ, Roger Williams Med Ctr, Dept Surg, Med Sch, 50 Maude St, Providence, RI 02908 USA; 3.Brown Univ, Rhode Isl Hosp, Dept Emergency Med, Dept Med, Providence, RI 02903 USA; 4.Northwestern Univ, Feinberg Cardiovasc Res Inst, Feinberg Sch Med, Chicago, IL 60611 USA; 5.Chinese Acad Sci, Inst Hlth Sci, Shanghai Inst Biol Sci, Key Lab Stem Cell Biol, Shanghai, Peoples R China; |
| 推荐引用方式 GB/T 7714 | Wang, Hao,Zhao, Yu,Wang, Jianguo,et al. Myocyte-specific overexpressing HDAC4 promotes myocardial ischemia/reperfusion injury[J]. MOLECULAR MEDICINE,2018,24(-):UNSP 37. |
| APA | Wang, Hao.,Zhao, Yu.,Wang, Jianguo.,Zhao, Ting C..,Zhang, Ling.,...&,.(2018).Myocyte-specific overexpressing HDAC4 promotes myocardial ischemia/reperfusion injury.MOLECULAR MEDICINE,24(-),UNSP 37. |
| MLA | Wang, Hao,et al."Myocyte-specific overexpressing HDAC4 promotes myocardial ischemia/reperfusion injury".MOLECULAR MEDICINE 24.-(2018):UNSP 37. |
入库方式： OAI收割
来源：上海营养与健康研究所
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