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Response gene to complement 32 regulates the G2/M phase checkpoint during renal
tubular epithelial cell repair
#MMPMID28536621
Shen YL
; Liu HJ
; Sun L
; Niu XL
; Kuang XY
; Wang P
; Hao S
; Huang WY
Cell Mol Biol Lett
2016[]; 21
(?): 19
PMID28536621
show ga
BACKGROUND: The aim of this study was to evaluate the influence of RGC-32
(response gene to complement 32) on cell cycle progression in renal tubular
epithelial cell injury. METHODS: NRK-52E cells with overexpressed or silenced
RGC-32 were constructed via transient transfection with RGC-32 expression plasmid
and RGC-32 siRNA plasmid, and the cell cycle distribution was determined. The
expression levels of fibrosis factors, including smooth muscle action (?-SMA),
fibronectin (FN) and E-cadherin, were assessed in cells with silenced RGC-32.
RESULTS: The cells were injured via TNF-? treatment, and the injury was
detectable by the enhanced expression of neutrophil gelatinase-associated
lipocalin (NGAL). RGC-32 expression also increased significantly. The number of
cells at G2/M phase increased dramatically in RGC-32 silenced cells, indicating
that RGC-32 silencing induced G2/M arrest. In addition, after treatment with
TNF-?, the NRK-52E cells with silenced RGC-32 showed significantly increased
expression of ?-SMA and FN, but decreased expression of E-cadherin. CONCLUSIONS:
The results of this study suggest that RGC-32 probably has an important impact on
the repair process of renal tubular epithelial cells in vitro by regulating the
G2/M phase checkpoint, cell fibrosis and cell adhesion. However, the exact
mechanism needs to be further elucidated.
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