Protein tyrosine phosphorylation in the ischemic brain.
Protein tyrosine phosphorylation in the ischemic brain.
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DOI：
10.1254/jphs.14r04cp
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发表时间：
2014-08
影响因子：
3.5
通讯作者：
N. Takagi
中科院分区：
文献类型：
--
作者：
N. Takagi
脑缺血是一种脑组织经历脑血流量不足的病理状况，与脑血管疾病、脑外伤、癫痫和心脏骤停相关。血流量的减少使脑组织得不到氧气和葡萄糖的供应，从而导致缺血核心中的细胞死亡以及随后的半影中的外周损伤。再灌注发生的半影区的神经元功能不活跃，但仍有活力。许多生物化学变化可导致神经元细胞死亡，从而诱发中枢神经系统功能障碍。然而，负责缺血性中风诱导的细胞损伤的机制仍有待确定。蛋白质磷酸化与脑中多种细胞反应的调节有关。最初，酪氨酸磷酸化被认为参与细胞生长和发育的调节。此外，发现脑中由酪氨酸磷酸化介导的各种突触和细胞功能与相对高水平的蛋白酪氨酸激酶活性相关。然而，这种蛋白酪氨酸激酶活性参与缺血性细胞死亡仍然没有完全了解。本文综述了蛋白酪氨酸磷酸化在缺血性脑中的可能意义。
Cerebral ischemia, a pathological condition in which brain tissue experiences a shortage of cerebral blood flow, is associated with cerebrovascular disease, brain trauma, epilepsy, and cardiac arrest. A reduction in blood flow leaves the brain tissue unsupplied with oxygen and glucose, thus leading to cell death in the ischemic core as well as subsequent peripheral injury in the penumbra. Neurons in the penumbra, where reperfusion occurs, are functionally inactive but still viable. Many biochemical changes, which may lead to neuronal cell death, thereby induce dysfunction of the central nervous system. However, the mechanisms responsible for ischemic stroke-induced cell damage remain to be determined. Protein phosphorylation has been implicated in the regulation of diverse cellular responses in the brain. Initially, tyrosine phosphorylation was considered to be involved in the regulation of cell growth and development. In addition, a variety of synaptic and cellular functions mediated by tyrosine phosphorylation in the brain were found to be associated with relatively high levels of protein tyrosine kinase activity. However, the involvement of this protein tyrosine kinase activity in ischemic cell death is still not fully understood. This review summarizes recent advances dealing with the possible implications of protein tyrosine phosphorylation in the ischemic brain.