Mestril R, Giordano F J, Conde A G, Dillmann W H
Department of Medicine, University of California, San Diego, La Jolla 92093-0618, USA.
J Mol Cell Cardiol. 1996 Dec;28(12):2351-8. doi: 10.1006/jmcc.1996.0228.
We have recently shown that the overexpression of a heat shock protein 70 (hsp 70) in a rat myogenic cell line confers protection against simulated ischemia. We also developed and demonstrated that overexpression of this protein, in the hearts of transgenic mice, protects against ischemia/reperfusion injury. We have now inserted the hsp70 gene in an adenoviral vector and show that we are able to transfer and achieve overexpression of this protein in neonatal cardiomyocytes and in the rat myogenic cell line H9c2. We find that cells infected with the adenoviral-hsp70i construct are rendered tolerant to simulated ischemia as compared to cells infected with a control recombinant adenoviral construct. In conclusion, our results demonstrate the feasibility of using adenoviral vectors to overexpress the hsp70 in myogenic cells, specially in cardiomyocytes, and the efficiency of this approach for providing protection against myocardial ischemia.
我们最近发现，大鼠成肌细胞系中热休克蛋白70（hsp 70）的过表达可赋予对模拟缺血的保护作用。我们还研发并证实，在转基因小鼠心脏中该蛋白的过表达可预防缺血/再灌注损伤。我们现已将hsp70基因插入腺病毒载体，并表明我们能够在新生心肌细胞和大鼠成肌细胞系H9c2中转移并实现该蛋白的过表达。我们发现，与感染对照重组腺病毒构建体的细胞相比，感染腺病毒-hsp70i构建体的细胞对模拟缺血具有耐受性。总之，我们的结果证明了使用腺病毒载体在成肌细胞，特别是心肌细胞中过表达hsp70的可行性，以及这种方法预防心肌缺血的有效性。
