title: Activation of the miR-17 family and miR-21 during murine kidney ischemia-reperfusion injury.
abstract: BACKGROUND
  Ischemia-reperfusion (I/R) is the main cause of acute kidney injury (AKI) in patients. We investigated renal microRNA (miRNA) expression profiles and the time course of changes in selected miRNA expressions after renal I/R to characterize the miRNA network activated during development and recovery from AKI.
  
  
  RESULTS
  One day after lethal (30 minutes) and sublethal (20 minutes) renal ischemia, AKI was verified by renal histology (tubular necrosis, regeneration), blood urea nitrogen (BUN) level, renal mRNA expression, and plasma concentration of neutrophil gelatinase-associated lipocalin (NGAL) in C57BL/6J mice. On the first day after 30-minute, lethal I/R miR-21, miR-17-5p, and miR-106a were elevated out of the 21 miRNAs successfully profiled on the Luminex multiplex assay. After 20-minute, sublethal I/R, renal miR-17-5p and miR-106a expressions were elevated on the first and second days of reperfusion, while miR-21 expression increased later and lasted longer. Renal miR-17-5p and miR-21 expressions correlated with each other. Renal function returned to normal on the fourth day after sublethal I/R.
  
  
  CONCLUSIONS
  Our results demonstrate that besides miR-21, miR-17-5p, and miR-106a are additionally activated during the maintenance and recovery phases of renal I/R injury. Furthermore, a correlation between renal miR-17-5p and miR-21 expressions warrants further investigation of how they may influence each other and the outcome of renal ischemia-reperfusion injury.
authors.affiliation: Institute of Pathophysiology, Semmelweis University, Budapest, Hungary.
authors.forename: Tamás
authors.initials: T
authors.lastname: Kaucsár
authors.forename: Csaba
authors.initials: C
authors.lastname: Révész
authors.forename: Mária
authors.initials: M
authors.lastname: Godó
authors.forename: Tibor
authors.initials: T
authors.lastname: Krenács
authors.forename: Mihály
authors.initials: M
authors.lastname: Albert
authors.forename: Csaba Imre
authors.initials: CI
authors.lastname: Szalay
authors.forename: László
authors.initials: L
authors.lastname: Rosivall
authors.forename: Zoltán
authors.initials: Z
authors.lastname: Benyó
authors.forename: Sándor
authors.initials: S
authors.lastname: Bátkai
authors.forename: Thomas
authors.initials: T
authors.lastname: Thum
authors.forename: Gábor
authors.initials: G
authors.lastname: Szénási
authors.forename: Péter
authors.initials: P
authors.lastname: Hamar
mesh_terms: D058186:Acute Kidney Injury / Q000209:etiology / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D000209:Acute-Phase Proteins / Q000235:genetics; D000818:Animals; D001806:Blood Urea Nitrogen; D005786:Gene Expression Regulation; D007668:Kidney / Q000378:metabolism / Q000473:pathology; D000071068:Lipocalin-2; D054834:Lipocalins / Q000097:blood / Q000235:genetics; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D035683:MicroRNAs / Q000235:genetics* / Q000378:metabolism; D015513:Oncogene Proteins / Q000097:blood / Q000235:genetics; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D015427:Reperfusion Injury / Q000150:complications / Q000235:genetics* / Q000378:metabolism / Q000473:pathology
chemical_list: D000209:Acute-Phase Proteins; D000071068:Lipocalin-2; D054834:Lipocalins; C531950:MIRN21 microRNA, mouse; D035683:MicroRNAs; C543896:Mirn106 microRNA, mouse; C543614:Mirn17 microRNA, mouse; D015513:Oncogene Proteins; D012333:RNA, Messenger; C071332:Lcn2 protein, mouse