通过转染特定热应激蛋白对原代大鼠心肌细胞的差异保护

Differential protection of primary rat cardiocytes by transfection of specific heat stress proteins.

作者信息

Cumming D V, Heads R J, Watson A, Latchman D S, Yellon D M

机构信息

Hatter Institute for Cardiovascular Studies, Department of Academic Cardiology, University College London Hospitals, London, UK.

出版信息

J Mol Cell Cardiol. 1996 Dec;28(12):2343-9. doi: 10.1006/jmcc.1996.0227.

DOI:10.1006/jmcc.1996.0227

PMID:9004151

Abstract

The aim of this study was to examine the individual contribution of specific heat stress proteins in primary rat cardiocytes to any protection observed following lethal heat stress or simulated lethal ischaemia. cDNAs for the inducible heat stress protein 70, for heat stress proteins 90 or 60, or a control plasmid were contransfected with a detectable marker, alkaline phosphatase, into cardiocytes. Survival assays were performed after the lethal stress. Transfection of the inducible heat stress protein 70 was found to increase survival following a lethal heat stress by 2.45-fold (P < 0.01) and against lethal ischaemia by 2.71-fold (P < 0.01). Transfection of heat stress protein 90 improved survival against heat by 2.55-fold (P < 0.05) but failed to have any effect on survival against lethal ischaemia. Transfection of heat stress protein 60 offered no protection against either stress.

摘要

本研究的目的是检测原代大鼠心肌细胞中特定热应激蛋白对致死性热应激或模拟致死性缺血后所观察到的任何保护作用的个体贡献。将诱导型热应激蛋白70、热应激蛋白90或60的cDNA，或对照质粒与可检测标记物碱性磷酸酶共转染到心肌细胞中。在致死性应激后进行存活分析。结果发现，转染诱导型热应激蛋白70可使致死性热应激后的存活率提高2.45倍（P<0.01），使致死性缺血后的存活率提高2.71倍（P<0.01）。转染热应激蛋白90可使抗热存活率提高2.55倍（P<0.05），但对致死性缺血后的存活率没有任何影响。转染热应激蛋白60对两种应激均无保护作用。