Kalirin-7, a protein enriched in postsynaptic density, is involved in ischemic signal transduction
Kalirin-7, a protein enriched in postsynaptic density, is involved in ischemic signal transduction
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DOI：
10.1007/s11064-008-9631-y
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发表时间：
2008-09-01
影响因子：
4.4
通讯作者：
Zablocka, Barbara
中科院分区：
文献类型：
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作者：
Beresewicz, Malgorzata;Kowalczyk, Joanna E.;Zablocka, Barbara
丝裂原活化蛋白激酶(MAPK)和c-jun氨基末端/应激激活蛋白(JNK)的调节因子包括Rho样小GTP结合蛋白及其调节因子。SynGAP和Kalirin-7是突触后密度丰富的蛋白，通过它们与Rho GTP酶和PSD-95支架蛋白的相互作用而被识别。我们检测了短暂性前脑缺血沙土鼠模型中SynGAP、Kalirin-7和PSD-95的免疫反应性、MAPK和JNK的磷酸化。在正常脑组织中，抗缺血的海马区CA2-3、DG中Kalirin-7的表达较高，而P-JNK的表达较低。缺血5min再灌流1h后，海马区P-ERK表达减少，P-JNK表达增加。相比之下，CA2-3、DG中Kalirin-7的含量达到对照的56%(P<；0.001)，而CA1中Kalirin-7的含量增加了一倍。与之相反，SynGAP在CA2-3、DG表达增强，在CA1表达减弱。我们的数据表明SynGAP和Kalirin-7参与了缺血信号转导的调节，但其机制似乎与MAPK和JNK的激活没有直接关系。
Regulators of mitogen activated protein kinases (MAPK) and c-Jun N-terminal/stress-activated kinase (JNK) include Rho-like small GTP-binding proteins and their regulators. SynGAP and kalirin-7 are postsynaptic density-enriched proteins identified through their interaction with Rho GTPases and PSD-95 scaffold protein. We examined immunoreactivity of SynGAP, kalirin-7, and PSD-95, phosphorylation of MAPK and JNK in control and postischemic hippocampus in gerbil model of transient forebrain ischemia. In normal brain higher amount of kalirin-7 but a lower amount of P-JNK was found in ischemia-resistant hippocampal area: CA2-3, DG than in ischemia-vulnerable CA1. After 5 min ischemia and 1 h reperfusion a decrease of P-ERK and increase of P-JNK were uniformly observed in the hippocampal parts. By contrast, the amount of kalirin-7 in CA2-3, DG reached 56% (P < 0.001) of control while was doubled in CA1. Oppositely, the immunoreactivity of SynGAP was increased in CA2-3, DG and reduced in CA1. Our data indicate that SynGAP and kalirin-7 take part in the regulation of ischemic signal transduction but the mechanism does not seem directly connected with the activation of MAPK and JNK.