ATF3在心肌缺血再灌注损伤中的负性调控作用

杨超君; 杨俊; 王辉波

doi:10.13201/j.issn.1001-1439.2015.08.004

ATF3在心肌缺血再灌注损伤中的负性调控作用

- 三峡大学心血管病研究所三峡大学第一临床医学院心内科(湖北宜昌, 443003)
基金项目:
国家自然科学基金（No：81170133，81200088，81470387）；湖北省医学领军人才

详细信息

通讯作者: 杨俊,E-mail:yangjun@medmail.com.cn

中图分类号: R541.4

收稿日期: 2014-12-18

修回日期: 2015-01-13

The negative regulatory factor in myocardial ischemia reperfusion injury of ATF3

- Cardiology Department, the First Affiliated Hospital of Three Gorges University, Yichang, Hubei, 443003, China

More Information

Corresponding author: YANG Jun, E-mail: yangjun@medmail.com.cn

Received Date: 18 December 2014

Revised Date: 13 January 2015

摘要

摘要: 冠心病是危害人类健康的疾病，近几十年来其发病率和病死率呈上升趋势。再灌注治疗是挽救心肌梗死的有效手段，同时也可能对心脏产生更大的损伤，即心肌缺血再灌注损伤（myocardial ischemia reperfusion injury，MIRI）。大量研究表明，ATF/CERB家族成员ATF3在缺血再灌注损伤中发挥负性调控作用。本文将对ATF3的表达特点和其在MIRI中的负性调控作用进行综述。这将为ATF3过表达治疗MIRI这一基因治疗策略提供理论基础。
- 心肌缺血再灌注损伤 /
- 转录激活因子3 /
- TLR4
Abstract: Coronary heart disease (CHD) is a disorder that endangers human health, which appears to rise in morbidity and mortality in recent decades. Reperfusion therapies are the effective strategies to rescue infracted myocardium, at the same time, these means of ischemia reperfusion may lead more serious injure in heart, which is called myocardial ischemia reperfusion injury (MIRI). Scores of researches demonstrated that ATF/CREB family member ATF3 developed a negative regulation in ischemia reperfusion injury (IRI). This review will expound the expression characteristic of ATF3 and its negative regulation in MIRI. Here, we may provide a theoretical basis that over expression ATF3 in myocardium is a promising gene therapeutic strategy in MIRI.
- myocardial ischemia reperfusion injury /
- activating transcrip tion factor /
- TLR4

HTML全文

参考文献(24)

[1]	GO A S, MOZAFFARIAN D, ROGER V L, et al. Executive summary:heart disease and stroke statistics-2014 update:a report from the American Heart Association[J]. Circulation, 2014, 129:399-410.
[2]	GILCHRIST M, THORSSON V, LI B, et al. Systems biology approaches identify ATF3 as a negative regulator of Toll-like receptor 4[J]. Nature, 2006, 441:173-178.
[3]	HAI T W, LIU F, COUKOS W J, et al. Transcription factor ATF cDNA clones:an extensive family of leucine zipper proteins able to selectively form DNA-binding heterodimers[J]. Genes Dev, 1989, 3:2083-2090.
[4]	CHEN B P, LIANG G, WHELAN J, et al. ATF3 and ATF3 delta Zip. Transcriptional repression versus activation by alternatively spliced isoforms[J]. J Biol Chem, 1994, 269:15819-15826.
[5]	HAI T, CURRAN T. Cross-family dimerization of transcription factors Fos/Jun and ATF/CREB alters DNA binding specificity[J]. Proc Natl Acad Sci U S A, 1991, 88:3720-3724.
[6]	HAI T, WOLFORD C C, CHANG Y S. ATF3, a hub of the cellular adaptive-response network, in the pathogenesis of diseases:is modulation of inflammation a unifying component?[J]. Gene Expr, 2010, 15:1-11.
[7]	YAMAMOTO S, YAMANE M, YOSHIDA O, et al. Activations of mitogen-activated protein kinases and regulation of their downstream molecules after rat lung transplantation from donors after cardiac death[J]. Transplant Proc, 2011, 43:3628-3633.
[8]	WANG L, DENG S, LU Y, et al. Increased inflammation and brain injury after transient focal cerebral ischemia in activating transcription factor 3 knockout mice[J]. Neuroscience, 2012, 220:100-108.
[9]	SONG D Y, OH K M, YU H N, et al. Role of activating transcription factor 3 in ischemic penumbra region following transient middle cerebral artery occlusion and reperfusion injury[J]. Neurosci Res, 2011, 70:428-434.
[10]	ZHANG T, ZHAO L L, CAO X, et al. Bioinformatics analysis of time series gene expression in left ventricle (LV) with acute myocardial infarction (AMI)[J]. Gene, 2014, 543:259-267.
[11]	KRIVORUCHKO A, STOREY K B. Activation of the unfolded protein response during anoxia exposure in the turtle Trachemys scripta elegans[J]. Mol Cell Biochem, 2013, 374:91-103.
[12]	DA SILVA R, LUCCHINETTI E, PASCH T, et al. Ischemic but not pharmacological preconditioning elicits a gene expression profile similar to unprotected myocardium[J]. Physiol Genomics, 2004, 20:117-130.
[13]	DELAROSA O, DALEMANS W, LOMBARDO E. Toll-like receptors as modulators of mesenchymal stem cells[J]. Front Immunol, 2012, 3:182.
[14]	GLUSHKOVA O V, KHRENOV M O, NOVOSELOVA T V, et al. The role of the NF-κB, SAPK/JNK, and TLR4 signalling pathways in the responses of RAW 264.7 cells to extremely low-intensity microwaves[J]. Int J Radiat Biol, 2015, 91:321-328.
[15]	WHITMORE M M, IPARRAGUIRRE A, KUBELKA L, et al. Negative Regulation of TLR-Signaling Pathways by Activating Transcription Factor-3[J]. J Immunol, 2007, 179:3622-3630.
[16]	NGUYEN C T, KIM E H, LUONG T T, et al. TLR4 Mediates Pneumolysin-Induced ATF3 Expression through the JNK/p38 Pathway in-Infected RAW 264.7 Cells[J]. Mol Cells, 2015, 38:58-64.
[17]	SUGANAMI T, YUAN X, SHIMODA Y, et al. Activating Transcription Factor 3 Constitutes a Negative Feedback Mechanism That Attenuates Saturated Fatty Acid/Toll-Like Receptor 4 Signaling and Macrophage Activation in Obese Adipose Tissue[J]. Circ Res, 2009, 105:25-32.
[18]	LI H F, CHENG C F, LIAO W J, et al. ATF3-mediated epigenetic regulation protects against acute kidney injury[J]. J Am Soc Nephrol, 2010, 21:1003-1013.
[19]	RAO J, QIAN X, LI G, et al. ATF3-Mediated NRF2/HO-1 Signaling Regulates TLR4 Innate Immune Responses in Mouse Liver Ischemia/Reperfusion Injury[J]. Am J Transplant, 2015, 15:76-87.
[20]	BROOKS A C, GUO Y, SINGH M, et al. Endoplasmic reticulum stress-dependent activation of ATF3 mediates the late phase of ischemic preconditioning[J]. J Mol Cell Cardiol, 2014, 76:138-147.
[21]	KIM H B, KONG M, KIM T M, et al. NFATc4 and ATF3 negatively regulate adiponectin gene expression in 3T3-L1 adipocytes[J]. Diabetes, 2006, 55:1342-1352.
[22]	KOUZARIDES T. Acetylation:a regulatory modification to rival phosphorylation?[J]. Embo J, 2000, 19:1176-1179.
[23]	ZHAO T C, CHENG G, ZHANG L X, et al. Inhibition of histone deacetylases triggers pharmacologic preconditioning effects against myocardial ischemic injury[J]. Cardiovasc Res, 2007, 76:473-481.
[24]	GRANGER A, ABDULLAH I, HUEBNER F, et al. Histone deacetylase inhibition reduces myocardial ischemia-reperfusion injury in mice[J]. FASEB J, 2008, 22:3549-3560.