@Article{biocell.2007.31.213,
AUTHOR = {LI KAILONG, DU XIAOLAN, HE YANI, ZHAO LIN, YANG JVRONG, SONG RUIHUA,  CHEN LIN},
TITLE = {p53-Rb signaling pathway is involved in tubular cell senescence in renal ischemia/reperfusion injury},
JOURNAL = {BIOCELL},
VOLUME = {31},
YEAR = {2007},
NUMBER = {2},
PAGES = {213--223},
URL = {http://www.techscience.com/biocell/v31n2/33929},
ISSN = {1667-5746},
ABSTRACT = {<b>Objective:</b> 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. <b>Methods:</b> 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. <b>Results:</b> 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. <b>Conclusion:</b> 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.
},
DOI = {10.32604/biocell.2007.31.213}
}