| Registro completo |
| Provedor de dados: |
Biocell
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| País: |
Argentina
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| Título: |
p53-Rb signaling pathway is involved in tubular cell senescence in renal ischemia/reperfusion injury
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| Autores: |
Li,Kailong
Du,Xiaolan
He,Yani
Zhao,Lin
Yang,Jvrong
Song,Ruihua
Chen,Lin
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| Data: |
2007-08-01
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| Ano: |
2007
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| Palavras-chave: |
Cell senescence
Cell cycle regulatory protein
Ischemia/reperfusion injury
Kidney
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| Resumo: |
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.
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| Tipo: |
Info:eu-repo/semantics/article
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| Idioma: |
Inglês
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| Identificador: |
http://www.scielo.org.ar/scielo.php?script=sci_arttext&pid=S0327-95452007000200003
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| Editor: |
Sociedad Latinoamericana de Microscopía Electrónica.; Centro Regional de Investigaciones Científicas y Tecnológicas (Mendoza, Argentina)
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| Formato: |
text/html
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| Fonte: |
Biocell v.31 n.2 2007
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| Direitos: |
info:eu-repo/semantics/openAccess
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