title: Stable expression of hypoxia-inducible factor-1α in human renal proximal tubular epithelial cells promotes epithelial to mesenchymal transition.
abstract: BACKGROUND
  Late kidney allograft dysfunction is becoming a significant problem and tubular atrophy and interstitial fibrosis are main causes. It was reported that hypoxia could induce epithelial-mesenchymal transition (EMT) in renal tubular epithelial cells (TECs), and hypoxia-inducible factor-1 (HIF-1) is one of the important regulators of cellular adaptive to hypoxia.
  
  
  METHODS
  In this study, we used an HIF-1αΔODD-expressing adenovirus, which could stably and functionally express HIF-1α under normoxia conditions, and used a hypoxia/reoxygenation cell model to simulate ischemia/reperfusion (I/R) injury in vitro, to investigate the effect of HIF-1α on EMT-related gene expressions.
  
  
  RESULTS
  Our results demonstrated that HIF-1α could significantly upregulate α-smooth muscle actin expression, and reduced the E-cadherin expression in HK-2 cells during I/R injury. Moreover, miR-21 expression had a positive correlation with HIF-1α in this process.
  
  
  CONCLUSIONS
  These results suggest that HIF-1α may promote the EMT development through regulating fibrotic gene expression during I/R injury in human renal TECs, and miR-21 could be among the important regulatory pathways in the process.
authors: Department of Research and Education, Guizhou Province People's Hospital, Guiyang, China.
authors: L
authors: L
authors: Luo
authors: Department of Urology Surgery, Guizhou Province People's Hospital, Guiyang, China.
authors: G
authors: G
authors: Luo
authors: Department of Nursing, Guizhou Province People's Hospital, Guiyang, China.
authors: Q
authors: Q
authors: Fang
authors: Department of Urology Surgery, Guizhou Province People's Hospital, Guiyang, China. Electronic address: szl7710@hotmail.com.
authors: Z
authors: Z
authors: Sun
mesh_terms: D000199:Actins / Q000378:metabolism; D000256:Adenoviridae / Q000235:genetics / Q000378:metabolism; D015703:Antigens, CD; D015820:Cadherins / Q000378:metabolism; D002460:Cell Line; D058750:Epithelial-Mesenchymal Transition; D005786:Gene Expression Regulation; D006085:Graft Survival; D006801:Humans; D000860:Hypoxia / Q000473:pathology; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000378:metabolism*; D007668:Kidney / Q000473:pathology; D016030:Kidney Transplantation; D007684:Kidney Tubules / Q000166:cytology*; D035683:MicroRNAs / Q000378:metabolism; D009130:Muscle, Smooth / Q000378:metabolism; D010100:Oxygen / Q000378:metabolism; D034622:RNA Interference; D015427:Reperfusion Injury; D015854:Up-Regulation
chemical_list: D000199:Actins; D015703:Antigens, CD; C513384:CDH1 protein, human; D015820:Cadherins; C497442:HIF1A protein, human; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; C524940:MIRN21 microRNA, human; D035683:MicroRNAs; D010100:Oxygen