LPS-stimulating astrocyte-conditioned medium causes neuronal apoptosis via increasing CDK11(p58) expression in PC12 cells through downregulating AKT pathway

Activation of astrocytes in central nervous system inflammation leads to a disturbance of crosstalk between astrocytes and neurons, and that this may contribute to the death of neurons. CDK11(p58) is a member of the large family of p34cdc2-related kinases. It specifically expresses in G2/M phase of...

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Bibliographic Details
Published in:Cellular and molecular neurobiology 2013-08, Vol.33 (6), p.779
Main Authors: Liu, Xiaojuan, Cheng, Chun, Shao, Bai, Wu, Xiaohong, Ji, Yuhong, Lu, Xiang, Shen, Aiguo
Format: Article
Language:English
Subjects:
Animals
Apoptosis - drug effects
Astrocytes - metabolism
Culture Media, Conditioned - pharmacology
Cyclin D3 - biosynthesis
Cyclin D3 - metabolism
Gene Knockdown Techniques
Lipopolysaccharides - pharmacology
Neurons - cytology
Neurons - drug effects
Neurons - metabolism
PC12 Cells
Proto-Oncogene Proteins c-akt - metabolism
Rats
Signal Transduction - drug effects
Up-Regulation - drug effects
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Summary:Activation of astrocytes in central nervous system inflammation leads to a disturbance of crosstalk between astrocytes and neurons, and that this may contribute to the death of neurons. CDK11(p58) is a member of the large family of p34cdc2-related kinases. It specifically expresses in G2/M phase of the cell cycle and is closely related to cell cycle arrest and apoptosis. Here, we show that astrocyte-conditioned medium stimulated by lipopolysaccharide upregulates CDK11(p58) expression and meanwhile causes neuronal apoptosis. CDK11(p58) knockdown in PC12 cells represses neuronal apoptosis. CDK11(p58) overexpression in PC12 cells promotes neuronal apoptosis. AKT signaling pathway is involved in CDK11(p58)-induced neuronal apoptosis process.
ISSN:1573-6830
1573-6830
DOI:10.1007/s10571-013-9945-4