Institutional Repository of Peking University School of Basic Medical Sciences
学科主题 | 基础医学 |
Overexpression of heat-shock protein 20 in rat heart myogenic cells confers protection against simulated ischemia/reperfusion injury | |
Zhu, YH; Wang, X | |
关键词 | reperfusion injury adenovirus apoptosis necrosis heat-shock proteins |
刊名 | ACTA PHARMACOLOGICA SINICA
![]() |
2005-09-01 | |
DOI | 10.1111/j.1745-7254.2005.00137.x |
卷 | 26期:9页:1076-1080 |
收录类别 | SCI |
文章类型 | Article |
WOS标题词 | Science & Technology |
类目[WOS] | Chemistry, Multidisciplinary ; Pharmacology & Pharmacy |
研究领域[WOS] | Chemistry ; Pharmacology & Pharmacy |
关键词[WOS] | ALPHA-B-CRYSTALLIN ; PROTEIN-KINASE-C ; SHOCK-PROTEIN ; HSP27 GENE ; EXPRESSION ; STRESS ; THERMORESISTANCE ; RESISTANCE ; MUSCLE |
英文摘要 | Aim: To explore whether overexpression of the small heat shock protein HSP20 in rat cardiomyocytes protects against simulated ischemia/reperfusion (SI/R) injury. Methods: Recombinant adenovirus expressing HSP20 was used to infect rat H9c2 cardiomyocytes at high efficiency, as assessed by green fluorescent protein. H9c2 cells were subjected to SI/R stress; survival was estimated through assessment of lactate dehydrogenase and cell apoptosis through caspase-3 activity. Results: Overexpression of HSP20 decreased lactate dehydrogenase release by 21.5% and caspase-3 activity by 58.8%. Pretreatment with the protein kinase C inhibitor Ro-31-8220 (0.1 mu mol/L) for 30 min before SI/R canceled the protective effect of HSP20. The selective mitochondrial K-ATP(+), channel inhibitor 5-hydroxydecanoate (100 mu mol/L) had a similar effect. However, the non-selective K-ATP(+), channel inhibitor glibenclamide (100 mu mol/L) had no significant effect. Conclusion: These data indicate that the protective effect of HSP20 in vitro is primarily due to reduced necrotic and apoptotic death of cardiomyocytes, possibly via the protein kinase C/mitochondrial K(+)ATP pathway. |
语种 | 英语 |
WOS记录号 | WOS:000231833000009 |
Citation statistics | |
文献类型 | 期刊论文 |
条目标识符 | http://ir.bjmu.edu.cn/handle/400002259/62835 |
Collection | 北京大学基础医学院 |
作者单位 | Peking Univ, Minist Educ, Basic Med Coll, Dept Physiol & Pathophysiol,Key Lab Mol Cardiovas, Beijing 100083, Peoples R China |
Recommended Citation GB/T 7714 | Zhu, YH,Wang, X. Overexpression of heat-shock protein 20 in rat heart myogenic cells confers protection against simulated ischemia/reperfusion injury[J]. ACTA PHARMACOLOGICA SINICA,2005,26(9):1076-1080. |
APA | Zhu, YH,&Wang, X.(2005).Overexpression of heat-shock protein 20 in rat heart myogenic cells confers protection against simulated ischemia/reperfusion injury.ACTA PHARMACOLOGICA SINICA,26(9),1076-1080. |
MLA | Zhu, YH,et al."Overexpression of heat-shock protein 20 in rat heart myogenic cells confers protection against simulated ischemia/reperfusion injury".ACTA PHARMACOLOGICA SINICA 26.9(2005):1076-1080. |
Files in This Item: | There are no files associated with this item. |
Items in the repository are protected by copyright, with all rights reserved, unless otherwise indicated.
Edit Comment