CDK11p58 Promotes Rat Astrocyte Inflammatory Response via Activating p38 and JNK Pathways Induced by Lipopolysaccharide
CDK11p58 Promotes Rat Astrocyte Inflammatory Response via Activating p38 and JNK Pathways Induced by Lipopolysaccharide
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DOI：
10.1007/s11064-011-0643-7
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发表时间：
2012-03-01
影响因子：
4.4
通讯作者：
Shen, Aiguo
中科院分区：
文献类型：
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作者：
Liu, Xiaojuan;Cheng, Chun;Shen, Aiguo
作为对中枢神经系统中各种神经损伤的反应，静止的星形胶质细胞变成反应性星形胶质细胞。星形胶质细胞是主要的神经胶质细胞亚型，并且是参与许多神经疾病（包括创伤、中风、衰老以及发育性、遗传性、特发性或获得性神经退行性疾病）的发病机制的重要效应物。CDK 11（p58）（Cyclin-dependent kinases 11 protein 58/PITSLRE）是一种与p34 cdc 2相关的蛋白激酶，在正常细胞周期进程中起重要作用。在LPS刺激过程中，星形胶质细胞CDK 11（p58）表达增加。诱导的CDK 11（p58）与星形胶质细胞炎症反应平行。通过小干扰RNA（siRNA）敲低CDK 11（p58）可降低LPS诱导的星形胶质细胞炎症反应，而过表达CDK 11（p58）可增强该过程。CDK 11（p58）通过激活p38和JNK MAPK途径发挥其功能。本研究表明，CDK 11（p58）可能是中枢神经系统（CNS）炎症中宿主防御的重要调节因子。
In response to a variety of neural damages in the CNS, quiescent astrocytes become reactive astrocytes. Astrocytes are the major glial subtype and are important effectors that participate in the pathogenesis of numerous neural disorders, including trauma, stroke, aging, and developmental, genetic, idiopathic or acquired neurodegenerative diseases. CDK11(p58) (Cyclin-dependent kinases 11 protein 58/PITSLRE) is a p34cdc2-related protein kinase that plays an important role in normal cell cycle progression. In the process of LPS stimulus, the expression of CDK11(p58) in astrocytes was increased. Induced CDK11(p58) was parallel to astrocyte inflammatory response. Knockdown of CDK11(p58) by small-interfering RNAs (siRNAs) reduced the LPS-induced astrocyte inflammatory response, while overexpression CDK11(p58) enhanced the process. CDK11(p58) exerted its functions via activating p38 and JNK MAPK pathways. This study delineates that CDK11(p58) may be a significant regulatory factor for host defenses in central nervous system (CNS) inflammation.