title: MicroRNA-21 attenuates renal ischemia reperfusion injury via targeting caspase signaling in mice.
abstract: BACKGROUND
  MicroRNAs (miR) have come into focus as powerful regulators of gene expression and potential diagnostic tools during renal ischemia reperfusion injury (IRI). The aim of this study was to investigate the molecular regulation and function of miR-21, and to analyze the relationship between caspases and miR-21 expression levels in an experimental model of renal IRI.
  
  
  METHODS
  IRI was induced by bilateral renal ischemia for 45 min followed by reperfusion. The male BALB/c mice were randomly assigned to the following groups: pre-miR-21 + IRI group, antagomiR-21 + IRI group, PBS + IRI group, pre-miR-21 + sham operation group, antagomiR-21 + sham operation group, PBS + sham operation group. The pre-miR-21 or antagomiR-21 was administered intraperitoneally (200 ng/kg weight) 24 and 6 h before induction of ischemia. Renal function, histological damage, renal cell apoptosis proteins were evaluated at 24 h after reperfusion.
  
  
  RESULTS
  Mice upregulated miR-21 had lower plasma levels of blood urea nitrogen (BUN) and creatinine, lower histopathological scores and a decrease in programmed cell death 4 (PDCD4) mRNA and active caspase-3, caspase-8 proteins expressions.
  
  
  CONCLUSIONS
  miR-21 is endowed with anti-apoptotic properties by suppressing the expression of PDCD4 gene and active caspase 3/8 fragments in the condition of renal IRI. miR-21 exerts significant functional protection in our renal murine model of IRI.
authors.affiliation: Department of Urology, The Second Affiliated Hospital of Nanchang University, Nanchang, PR China.
authors.forename: Honglin
authors.initials: H
authors.lastname: Hu
authors.forename: Wei
authors.initials: W
authors.lastname: Jiang
authors.forename: Xiaoqing
authors.initials: X
authors.lastname: Xi
authors.forename: Cong
authors.initials: C
authors.lastname: Zou
authors.forename: Zhenfeng
authors.initials: Z
authors.lastname: Ye
mesh_terms: D000818:Animals; D017209:Apoptosis; D051017:Apoptosis Regulatory Proteins / Q000378:metabolism; D001806:Blood Urea Nitrogen; D053148:Caspase 3 / Q000378:metabolism; D053181:Caspase 8 / Q000378:metabolism; D020169:Caspases / Q000378:metabolism*; D004195:Disease Models, Animal; D020869:Gene Expression Profiling; D020382:Interleukin-18 / Q000097:blood; D007511:Ischemia / Q000378:metabolism*; D007668:Kidney / Q000378:metabolism / Q000473:pathology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D035683:MicroRNAs / Q000235:genetics* / Q000378:metabolism*; D016601:RNA-Binding Proteins / Q000378:metabolism; D011897:Random Allocation; D015427:Reperfusion Injury / Q000473:pathology*; D015398:Signal Transduction; D015854:Up-Regulation
chemical_list: D051017:Apoptosis Regulatory Proteins; D053148:Caspase 3; D053181:Caspase 8; D020169:Caspases; D020382:Interleukin-18; D035683:MicroRNAs; D016601:RNA-Binding Proteins; C531950:MIRN21 microRNA, mouse; C498443:Pdcd4 protein, mouse; C505409:Casp3 protein, mouse; C505526:Casp8 protein, mouse