Chen Min, Hou XiaoYu, Zhang GuangYi
Research Center for Biochemistry and Molecular Biology, Xuzhou Medical College, 84 West Huai-hai Road, Xuzhou, 221002 P.R., Jiangsu, China.
Neurosci Lett. 2003 Mar 13;339(1):29-32. doi: 10.1016/s0304-3940(02)01439-8.
In this study, we investigated the effects of protein tyrosine kinase (PTK) and protein tyrosine phosphatase (PTP) on the tyrosine phosphorylation of N-methyl-D-aspartate receptor subunit 2A (NR2A) and the interactions among NR2A, postsynaptic density protein 95 (PSD-95), Fyn/Src after brain ischemia/reperfusion (I/R). The following results were observed: (1) the increase in tyrosine phosphorylation of NR2A induced by I/R was suppressed by genistein, an inhibitor of PTK, but was further enhanced by sodium orthovanadate, an inhibitor of PTP, which were administered to the SD rats 20 min before ischemia. (2) Importantly, genistein and sodium orthovanadate increased and decreased the interactions involving NR2A, PSD-95, Fyn and Src, respectively. These results demonstrated that PTK and PTP were involved in regulating tyrosine phosphorylation of NR2A through changing the interaction among NR2A, PSD-95, Fyn/Src.
在本研究中，我们研究了蛋白酪氨酸激酶（PTK）和蛋白酪氨酸磷酸酶（PTP）对脑缺血/再灌注（I/R）后N-甲基-D-天冬氨酸受体2A亚基（NR2A）酪氨酸磷酸化的影响，以及NR2A、突触后致密蛋白95（PSD-95）、Fyn/Src之间的相互作用。观察到以下结果：（1）PTK抑制剂染料木黄酮抑制了I/R诱导的NR2A酪氨酸磷酸化增加，但PTP抑制剂原钒酸钠在缺血前20分钟给予SD大鼠后，进一步增强了该磷酸化。（2）重要的是，染料木黄酮和原钒酸钠分别增加和减少了涉及NR2A、PSD-95、Fyn和Src的相互作用。这些结果表明，PTK和PTP通过改变NR2A、PSD-95、Fyn/Src之间的相互作用参与调节NR2A的酪氨酸磷酸化。
