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10.1038/s41598-017-10271-8

http://scihub22266oqcxt.onion/10.1038/s41598-017-10271-8
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C5579259!5579259!28860615
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suck abstract from ncbi


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pmid28860615      Sci+Rep 2017 ; 7 (ä): ä
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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[]; 7 (ä): ä PMID28860615show ga
  • The deletion of microsomal prostaglandin E synthase-2 (mPGES-2) does not affect in vivo PGE2 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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