Targeted hsp70.1 disruption increases infarction volume after focal cerebral ischemia in mice
Targeted hsp70.1 disruption increases infarction volume after focal cerebral ischemia in mice
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DOI：
10.1161/hs1201.099604
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发表时间：
2001-12-01
期刊：
影响因子：
8.3
通讯作者：
Seo, JS
中科院分区：
文献类型：
--
作者：
Lee, SH;Kim, M;Seo, JS
背景与目的热休克蛋白（Heat shock proteins，HSPs）是一类高度保守的蛋白质，在多种逆境胁迫下被诱导表达。HSP 70是一个70 kDa的HSP家族，已知对各种损伤具有细胞保护作用。HSP 70在脑缺血中的作用仍有待阐明在vivo. Methods-为了研究减少HSP 70水平对脑缺血的影响，局灶性脑缺血由大脑中动脉的管腔内闭塞诱导hsp70.1基因敲除小鼠。测定hsp70.1和hsp70.3 mRNA及HSP 70蛋白的表达，并测量和比较梗死体积。hsp70.1基因敲除小鼠的平均梗死体积（92.5 ± 8.3 mm（3））显著大于野生型小鼠（59.3 ± 8.9 mm，（3）P
Background and Purpose-Heat-shock proteins (HSPs) are highly conserved proteins that are induced by a variety of stresses. HSP70 is a 70-kDa HSP family known to have cytoprotective effects against various insults. The role of HSP70 in cerebral ischemia remains to be elucidated in vivo.Methods-To investigate the effect of reduced HSP70 levels on cerebral ischemia, focal cerebral ischemia by intraluminal occlusion of the middle cerebral artery was induced in hsp70.1 knockout mice. The expressions of hsp70.1 and hsp70.3 mRNAs and HSP70 protein were determined, and infarction volumes were measured and compared.Results-Northern blots confirmed the absence of hsp70.1 mRNA expression in the knockout mice. The mean infarction volume was significantly larger in hsp70.1 knockout mice (92.5 +/-8.3 mm(3)) than in the wild-type mice (59.3 +/-8.9 mm,(3) P