These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: P53-Rb signaling pathway is involved in tubular cell senescence in renal ischemia/reperfusion injury.
    Author: Kailong L, Du X, Yani H, Lin Z, Jvrong Y, Ruihua S, Lin C.
    Journal: Biocell; 2007 Aug; 31(2):213-23. PubMed ID: 17902269.
    Abstract:
    OBJECTIVE: To investigate the course of tubular cell senescence and expressions of p53, p21, and Rb during the late phase of ischemia/reperfusion (IRI) in the kidney, and assess the effects of the p53-Rb pathway on tubular cell senescence. METHODS: Experimental models of unilateral renal IRI were used in p53 (+/+) and p53 (-/-) mice. Histological changes at the tubular level, progress of cell senescence, and the expression of Rb, p21, and/or p53 proteins in tubular cells were studied at different moments in time after IRI. RESULTS: Chronic tubulointerstitial fibrosis was much more severe and widely distributed in IRI kidneys of p53 (+/+) mice in later stages than in earlier stages. Senescent tubular cells were significantly increased at 3 and 6 months after IRI. In contrast, in contralateral kidneys of p53 (+/+) mice and in both kidneys of p53 (-/-) mice, almost no senescent cells were observed at 1 and 3 months after IRI, and only a few senescent cells were detected in IRI kidneys of p53 (-/-) mice at 6 months. In mice of both genotypes, cell senescence was correlated with the expression levels of p53, p21, and Rb proteins. CONCLUSION: The IRI accelerated tubular cell senescence is presumed to be one of the mechanisms of the "long-term effect" of IRI. Furthermore, the activation of p53-Rb signaling pathway may play a vital role in tubular cell senescence induced by IRI.
    [Abstract] [Full Text] [Related] [New Search]