TY - EJOU
AU - KAILONG, LI
AU - XIAOLAN, DU
AU - YANI, HE
AU - LIN, ZHAO
AU - JVRONG, YANG
AU - RUIHUA, SONG
AU - LIN, CHEN
TI - p53-Rb signaling pathway is involved in tubular cell senescence in renal ischemia/reperfusion injury
T2 - BIOCELL
PY - 2007
VL - 31
IS - 2
SN - 1667-5746
AB - 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.
KW - cell senescence
KW - cell cycle regulatory protein
KW - ischemia/reperfusion injury
KW - kidney
DO - 10.32604/biocell.2007.31.213