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 beta-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-alpha release was enhanced in p21(Cip1-/-)microglial cells. In addition glial activation induced by lipopolysaccharide and the fibrillar form of the 1-42 beta-amyloid peptide upregulated p21(Cip1). Our results support a role for p21(Cip1) in the activation of glial cells, particularly in microglia.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
