Absence of the cell cycle inhibitor p21Cip1 reduces LPS-induced NO release and activation of the transcription factor NF-κB in mixed glial cultures
✍ Scribed by Josep Maria Tusell; Josep Saura; Joan Serratosa
- Publisher
- John Wiley and Sons
- Year
- 2004
- Tongue
- English
- Weight
- 149 KB
- Volume
- 49
- Category
- Article
- ISSN
- 0894-1491
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✦ Synopsis
Abstract
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.