Delayed phosphorylation of p38 mitogen-activated protein kinase in the AT1a knock-out mouse striatal neurons during middle cerebral artery occlusion and reperfusion

NEUROSCIENCE LETTERS

卷:341

Article

Hattori, H ; Shibata, M ; Sugaya, T ; Hamada, J ; Fukuuchi, Y

关键词: angiotensin;    angiotensin II receptor type 1a;    cerebral ischernia and reperfusion;    delayed neuronal death;    knock-out mouse;    microglia;    p38 mitogen-activated protein kinase;    proline-rich tyrosine kinase 2;   

DOI  :  10.1016/S0304-3940(03)00078-8

来源: Elsevier

【 摘 要 】

To investigate whether the phosphorylation of p38 in cerebral ischemia occurs via angiotensin It receptor type I a (AT 1 a), we examined the time course of phosphorylation of p38 and proline-rich tyrosine kinase 2 in AT1a knock-out mouse striatal neurons during middle cerebral artery occlusion (MCAO) and reperfusion. Phosphorylated-p38 was observed after 2 h and 5 h of reperfusion after I h of MCAO in C57/B6 mice and AT1a knock out mice, respectively. We demonstrated a delay of phosphorylation of p38 in the reperfusion model of the AT1a knock-out mouse, and detected microglia. in the striatum on the ischemic side that were phosphorylated-p38-positive after 71 h of reperfusion in both animals. However, there was no association between AT1a and delayed neuronal cell death, or between AT1a and activation of caspase-9 in cerebral ischemia/reperfusion. (C) 2003 Elsevier Science Ireland Ltd. All rights reserved.

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