Upregulation of p21Cip1 in activated glial cells

✍ Scribed by Josep Maria Tusell; Aroa Ejarque-Ortiz; Pilar Mancera; Carme Solà; Josep Saura; Joan Serratosa

• Publisher: John Wiley and Sons
• Year: 2009
• Tongue: English
• Weight: 553 KB
• Volume: 57
• Category: Article
• ISSN: 0894-1491
• DOI: 10.1002/glia.20781

✦ Synopsis

Abstract

The cdk inhibitor p21^Cip1^, also named p21^Cip1/Waf1^, is intimately involved in coupling growth arrest to cellular differentiation in several cell types. p21^Cip1^ is a multifunctional protein that might regulate cell‐cycle progression at different levels. In a recent study, we found no differences in the rate of proliferation between glial cells from wild‐type and p21^Cip1−/−^ mice. In the present study, we examined differences in glial activation between glial cells from wild‐type and p21^Cip1−/−^ mice, using mixed glial cultures, microglia‐enriched cultures, and astrocyte‐enriched cultures. We compared the effect of lipopolysaccharide and two forms (oligomeric and fibrillar) of the 1‐42 β‐amyloid peptide on glial activation. We observed an attenuation of nuclear translocation of the nuclear factor kappa‐B in p21^Cip1−/−^ glial cells, when compared with glial cells from wild‐type mice. In contrast, tumor necrosis factor‐α release was enhanced in p21^Cip1−/−^microglial cells. In addition glial activation induced by lipopolysaccharide and the fibrillar form of the 1‐42 β‐amyloid peptide upregulated p21^Cip1^. Our results support a role for p21^Cip1^ in the activation of glial cells, particularly in microglia. © 2008 Wiley‐Liss, Inc.