Edinburgh Research Explorer

miR-21 and miR-214 are consistently modulated during renal injury in rodent models

Research output: Contribution to journalArticle

  • Laura Denby
  • Vasudev Ramdas
  • Martin W McBride
  • Joe Wang
  • Hollie Robinson
  • John McClure
  • Wendy Crawford
  • Ruifang Lu
  • Dianne Z Hillyard
  • Raya Khanin
  • Reuven Agami
  • Anna F Dominiczak
  • Claire C Sharpe
  • Andrew H Baker

Related Edinburgh Organisations

Original languageEnglish
Pages (from-to)661-72
Number of pages12
JournalAmerican Journal of Pathology
Issue number2
Publication statusPublished - Aug 2011


Transforming growth factor (TGF)-β is one of the main fibrogenic cytokines that drives the pathophysiology of progressive renal scarring. MicroRNAs (miRNAs) are endogenous non-coding RNAs that post-transcriptionally regulate gene expression. We examined the role of TGF-β-induced expression of miR-21, miRNAs in cell culture models and miRNA expression in relevant models of renal disease. In vitro, TGF-β changed expression of miR-21, miR-214, and miR-145 in rat mesangial cells (CRL-2753) and miR-214, miR-21, miR-30c, miR-200b, and miR-200c during induction of epithelial-mesenchymal transition in rat tubular epithelial cells (NRK52E). miR-214 expression was robustly modulated in both cell types, whereas in tubular epithelial cells miR-21 was increased and miR-200b and miR-200c were decreased by 58% and 48%, respectively, in response to TGF-β. TGF-β receptor-1 was found to be a target of miR-200b/c and was down-regulated after overexpression of miR-200c. To assess the differential expression of these miRNAs in vivo, we used the anti-Thy1.1 mesangial glomerulonephritis model and the unilateral ureteral obstruction model in which TGF-β plays a role and also a genetic model of hypertension, the stroke-prone spontaneously hypertensive rat with and without salt loading. The expressions of miR-214 and miR-21 were significantly increased in all in vivo models, showing a possible miRNA signature of renal damage despite differing causes.

    Research areas

  • Animals, Disease Models, Animal, Gene Expression Regulation, Glomerulonephritis, Hypertension, Kidney, Kidney Glomerulus, Kidney Tubules, Male, MicroRNAs, Rats, Rats, Inbred WKY, Time Factors, Transforming Growth Factor beta, Ureter

ID: 23489740