CDK11(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, 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.