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Absence of the cell cycle inhibitor p21 Cip1 reduces LPS‐induced NO release and activation of the transcription factor NF‐κB in mixed glial cultures
Author(s) -
Tusell Josep Maria,
Saura Josep,
Serratosa Joan
Publication year - 2004
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.20095
Subject(s) - biology , transcription factor , microbiology and biotechnology , nfkb1 , transcription (linguistics) , nf κb , cell cycle , cell culture , cancer research , cell , signal transduction , genetics , gene , linguistics , philosophy
We have studied possible differences in glial activation between cells from wild‐type and p21 Cip1−/− 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 p21 Cip1−/− 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‐α (TNF‐α) release, and nuclear factor kappa‐B (NF‐κB) activation were evaluated as indicators of glial activation. We observed an attenuation of NO release and NF‐κB activation in p21 Cip1−/− glial cells when compared with glial cells from wild‐type mice. In contrast, TNF‐α release was enhanced in p21 Cip1−/− glia. These results suggest that the cell cycle inhibitor p21 Cip1 plays a role in the inflammatory response induced by LPS. © 2004 Wiley‐Liss, Inc.