TargetRx Atlas

MRNA basic information

  • mRNA ID:ENST00000257435
  • Gene Name:NREP
  • mRNA database:Ensembl
  • mRNA expression :up-regulated
  • mRNA Method:qRT-PCR
  • mRNA Pathway:miR-7a-5p/P311/TGF-β1 pathway
  • Evidence:validated
  • (mRNA-drug)

Drug basic information

  • Drug ID:DB03568
  • Drug Name:Butyric Acid
  • Drug Method:up-regulated the gene expression

Disease basic infommation

  • Disease:diabetic kidney disease
  • Tissue:cells line SV40-MES-13

Other information

  • Title:Butyrate alleviates diabetic kidney disease by mediating the miR-7a-5p/P311/TGF-β1 pathway
  • Journal:Faseb Journal
  • Published:2020
  • PubMed ID:32539181
  • Abstract:It has been reported that butyrate played an protect role in diabetic kidney disease (DKD) while the mechanism was still not clear. Transforming growth factor-β1 (TGF-β1) is the initial factor which triggers the profibrotic signaling cascades. P311 is an RNA-binding protein, which could stimulate TGF-β1 translation in several cell types. In our study, we found that supplementary of butyrate alleviated fibrosis and suppressed the expression of TGF-β1 and P311 in the kidney of db/db mice as well as high glucose (HG)-induced SV40-MES-13 cells. Overexpression of P311 offset the inhibition of butyrate on TGF-β1 in SV40-MES-13 cells. To make clear the mechanism of butyrate in regulating P311, microRNAs (miRNAs) of the SV40-MES-13 cells were sequenced. We found that miR-7a-5p was significantly decreased in the HG-induced SV40-MES-13 cells and the kidney of db/db mice, while giving butyrate reversed this change. Besides, miR-7a-5p could specifically target the 3' UTR of P311's mRNA and suppressed the expression of P311 in the SV40-MES-13 cells. Giving miR-7a-5p inhibitor blocked the inhibition of butyrate on P311 and TGF-β1. Introducing the miR-7a-5p agomir into db/db mice alleviated renal fibrosis and inhibit the expression of P311 and TGF-β1. In conclusion, butyrate alleviated DKD by mediating the miR-7a-5p/P311/TGF-β1 pathway.