Absence of the cell cycle inhibitor p21Cip1 reduces LPS-induced NO release and activation of the transcription factor NF-kappaB in mixed glial cultures

Glia
Josep Maria TusellJoan Serratosa

Abstract

We have studied possible differences in glial activation between cells from wild-type and p21Cip1-/- mice. We compared the effect of serum mitogenic stimulation on proliferation rate and on the total number of glial cells after 7 days of culture. No differences between wild-type and p21Cip1-/- glial cells were observed. We also compared the effect of lipopolysaccharide (LPS) from Escherichia coli, an agent widely used to induce glial activation. Nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha) release, and nuclear factor kappa-B (NF-kappaB) activation were evaluated as indicators of glial activation. We observed an attenuation of NO release and NF-kappaB activation in p21Cip1-/- glial cells when compared with glial cells from wild-type mice. In contrast, TNF-alpha release was enhanced in p21Cip1-/- glia. These results suggest that the cell cycle inhibitor p21Cip1 plays a role in the inflammatory response induced by LPS.

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Citations

Jan 8, 2013·Journal of the American Chemical Society·Yi-Ping ChenChung-Yuan Mou
Jul 4, 2012·Molecular and Cellular Biology·Bryce VincentZhengxin Wang
Feb 2, 2008·American Journal of Respiratory Cell and Molecular Biology·Hongwei YaoIrfan Rahman
Sep 25, 2008·Glia·Josep Maria TusellJoan Serratosa
Oct 31, 2016·Journal of Cellular Physiology·Amir BeinBetty Schwartz
Apr 20, 2017·Molecular Neurobiology·Bruna BellaverAndré Quincozes-Santos

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