CDK11 super(p58) Promotes Rat Astrocyte Inflammatory Response via Activating p38 and JNK Pathways Induced by Lipopolysaccharide

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, i...

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Bibliographic Details
Published in:Neurochemical research 2012-03, Vol.37 (3), p.563-573
Main Authors: Liu, Xiaojuan, Cheng, Chun, Shao, Bai, Wu, Xiaohong, Ji, Yuhong, Liu, Yichang, Lu, Xiang, Shen, Aiguo
Format: Article
Language:English
Subjects:
Aging
Astrocytes
c-Jun amino-terminal kinase
Cell cycle
Central nervous system
Cyclin-dependent kinase
Developmental genetics
Inflammation
Lipopolysaccharides
MAP kinase
Neurodegenerative diseases
Neuronal-glial interactions
Protein kinase
siRNA
Stroke
Trauma
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Summary: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 super(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 super(p58) in astrocytes was increased. Induced CDK11 super(p58) was parallel to astrocyte inflammatory response. Knockdown of CDK11 super(p58) by small-interfering RNAs (siRNAs) reduced the LPS-induced astrocyte inflammatory response, while overexpression CDK11 super(p58) enhanced the process. CDK11 super(p58) exerted its functions via activating p38 and JNK MAPK pathways. This study delineates that CDK11 super(p58) may be a significant regulatory factor for host defenses in central nervous system (CNS) inflammation.
ISSN:0364-3190
1573-6903
DOI:10.1007/s11064-011-0643-7