MicroRNA-21 protects from mesangial cell proliferation induced by diabetic nephropathy in db/db mice

FEBS Lett. 2009 Jun 18;583(12):2009-14. doi: 10.1016/j.febslet.2009.05.021. Epub 2009 May 19.


Diabetic nephropathy (DN) is a major diabetic complication. But the initiating molecular events triggering DN are unknown. Recent researches have addressed the role of microRNAs in diabetes and its complications. In this study, we looked for microRNAs expression during early DN, and showed microRNA-21 (miR-21) expression was downregulated in response to early DN in vitro and in vivo. Over-expression of miR-21 inhibited proliferation of mesangial cells and decreased the 24-h urine albumin excretion rate in diabetic db/db mice. Moreover, we identified PTEN as a target of miR-21. We also found PI3K and p-Akt increased in miR-21 treated mesangial cells and db/db mice. Overall, these studies for the first time provide evidence for the potential role of miR-21 in early DN.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Base Sequence
  • Cell Proliferation
  • Cells, Cultured
  • Diabetic Nephropathies / genetics*
  • Diabetic Nephropathies / metabolism
  • Diabetic Nephropathies / pathology*
  • Down-Regulation
  • Mesangial Cells / pathology*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Mutant Strains
  • MicroRNAs / genetics*
  • PTEN Phosphohydrolase / genetics
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • Signal Transduction
  • Transfection


  • MIRN21 microRNA, mouse
  • MicroRNAs
  • Phosphatidylinositol 3-Kinases
  • Proto-Oncogene Proteins c-akt
  • PTEN Phosphohydrolase
  • Pten protein, mouse