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Aggravation of acute kidney injury by mPGES-2 down regulation is associated with
autophagy inhibition and enhanced apoptosis
#MMPMID28860615
Li T
; Liu Y
; Zhao J
; Miao S
; Xu Y
; Liu K
; Liu M
; Wang G
; Xiao X
Sci Rep
2017[Aug]; 7
(1
): 10247
PMID28860615
show ga
The deletion of microsomal prostaglandin E synthase-2 (mPGES-2) does not affect
in vivo PGE(2) production, and the function of this enzyme remains unknown until
now. This study investigated the expression and roles of mPGES-2 in LPS induced
acute kidney injury (AKI) both in vitro and in vivo. We found that mPGES-2 was
up-regulated in kidney of mice with LPS induced AKI. Inhibition of mouse mpges2
gene expression exacerbated LPS-induced renal dysfunction, renal tubular cell
damage and apoptosis, while inhibited kidney autophagy. Further cellular
experiments showed that over-expression of mPGES-2 resulted in increased
autophagy and decreased apoptosis rate of renal tubular epithelial cells. In
addition, treatment with autophagy inhibitor 3-methyladenine could reverse the
above-mentioned results. On the contrary, interference of mPGES-2 expression by
siRNA decreased autophagy level but significantly increased apoptosis of tubular
epithelial cells and treatment with autophagy inducer rapamycin can reverse these
results. Overall, our study shows that mPGES-2 can protect renal tubular
epithelial cells by regulating autophagy levels and aggravation of acute kidney
injury by mPGES-2 down regulation is associated with autophagy inhibition and
enhanced apoptosis.
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