Intermittent hypoxia protects cardiomyocytes against ischemia-reperfusion injury-induced alterations in ca2+ homeostasis and contraction via the sarcoplasmic reticulum and na+/ca2+ exchange mechanisms
文献类型：期刊论文
| 作者 | Chen, L; Lu, XY; Li, J; Fu, JD; Zhou, ZN; Yang, HT |
| 刊名 | American journal of physiology-cell physiology
 |
| 出版日期 | 2006-04-01 |
| 卷号 | 290期号:4页码:C1221-c1229 |
| 关键词 | Intracellular ca2+ concentration Ca2+ transients Ca2+ transporters Myofilament ca2+ sensitivity |
| ISSN号 | 0363-6143 |
| DOI | 10.1152/ajpcell.00526.2005. |
| 通讯作者 | Yang, ht() |
| 英文摘要 | We have previously demonstrated that intermittent high-altitude (iha) hypoxia significantly attenuates ischemia-reperfusion (i/r) injury-induced excessive increase in resting intracellular ca2+ concentrations ([ca2+](i)). because the sarcoplasmic reticulum (sr) and na+/ca2+ exchanger (ncx) play crucial roles in regulating [ca2+](i) and both are dysfunctional during i/r, we tested the hypothesis that iha hypoxia may prevent i/r-induced ca2+ overload by maintaining ca2+ homeostasis via sr and ncx mechanisms. we thus determined the dynamics of ca2+ transients and cell shortening during preischemia and i/r injury in ventricular cardiomyocytes from normoxic and iha hypoxic rats. iha hypoxia did not affect the preischemic dynamics of ca2+ transients and cell shortening, but it significantly suppressed the i/r-induced increase in resting [ca2+](i) levels and attenuated the depression of the ca2+ transients and cell shortening during reperfusion. moreover, iha hypoxia significantly attenuated i/r- induced depression of the protein contents of sr ca2+ release channels and/or ryanodine receptors (ryrs) and sr ca2+ pump atpase (serca2) and sr ca2+ release and uptake. in addition, a delayed decay rate time constant of ca2+ transients and cell shortening of ca2+ transients observed during ischemia was accompanied by markedly inhibited ncx currents, which were prevented by iha hypoxia. these findings indicate that iha hypoxia may preserve ca2+ homeostasis and contraction by preserving ryrs and serca2 proteins as well as ncx activity during i/r. |
| WOS关键词 | PIG VENTRICULAR MYOCYTES ; SITE PHOSPHOLAMBAN PHOSPHORYLATION ; RAT-HEART ; INCREASED EXPRESSION ; CELLULAR MECHANISMS ; INTRACELLULAR CA2+ ; STUNNED MYOCARDIUM ; NA+-CA2+ EXCHANGER ; CALCIUM OVERLOAD ; GENE-EXPRESSION |
| WOS研究方向 | Cell Biology ; Physiology |
| WOS类目 | Cell Biology ; Physiology |
| 语种 | 英语 |
| WOS记录号 | WOS:000236573300031 |
| 出版者 | AMER PHYSIOLOGICAL SOC |
| URI标识 | http://www.irgrid.ac.cn/handle/1471x/2379488 |
| 专题 | 中国科学院大学 |
| 通讯作者 | Yang, HT |
| 作者单位 | 1.Chinese Acad Sci, Shanghai Inst Biol Sci, Mol Cardiol Lab, Inst Hlth Sci, Shanghai 200025, Peoples R China 2.Shanghai Jiao Tong Univ, Sch Med, Grad Sch, CAS, Shanghai 200025, Peoples R China 3.Shanghai Jiao Tong Univ, Sch Med, Mol Cardiol Lab, Inst Hlth Sci, Shanghai 200025, Peoples R China 4.Chinese Acad Sci, Shanghai Inst Biol Sci, Physiol Lab Hypoxia, Shanghai 200025, Peoples R China |
| 推荐引用方式 GB/T 7714 | Chen, L,Lu, XY,Li, J,et al. Intermittent hypoxia protects cardiomyocytes against ischemia-reperfusion injury-induced alterations in ca2+ homeostasis and contraction via the sarcoplasmic reticulum and na+/ca2+ exchange mechanisms[J]. American journal of physiology-cell physiology,2006,290(4):C1221-c1229. |
| APA | Chen, L,Lu, XY,Li, J,Fu, JD,Zhou, ZN,&Yang, HT.(2006).Intermittent hypoxia protects cardiomyocytes against ischemia-reperfusion injury-induced alterations in ca2+ homeostasis and contraction via the sarcoplasmic reticulum and na+/ca2+ exchange mechanisms.American journal of physiology-cell physiology,290(4),C1221-c1229. |
| MLA | Chen, L,et al."Intermittent hypoxia protects cardiomyocytes against ischemia-reperfusion injury-induced alterations in ca2+ homeostasis and contraction via the sarcoplasmic reticulum and na+/ca2+ exchange mechanisms".American journal of physiology-cell physiology 290.4(2006):C1221-c1229. |
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来源：中国科学院大学
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