Overexpression of megsin induces mesangial cell proliferation and excretion of type IV collagen in vitro

Cell Immunol. 2011;271(2):413-7. doi: 10.1016/j.cellimm.2011.08.009. Epub 2011 Sep 5.


Over-expression of megsin is associated with mesangial cell (MC) proliferation and extracellular matrix (ECM) accumulation. The underlying pathogenesis is unknown. This study demonstrate that over-expression of megsin induced incorporation of [(3)H]thymidine in MCs and PDGF-BB, TGF-β1 upregulation. Concentrations of PDGF-BB, TGF-β1 and type IV collagen in the culture medium of MCs transfected with megsin were higher than controls. Anti-PDGF-BB suppressed incorporation of [(3)H]thymidine in MCs transfected with megsin and mRNA expression of TGF-β1 in stable transformant MCs, suggesting that over-expression of megsin induces cell proliferation and ECM accumulation in MCs, upregulation of PDGF-BB and TGF-β1 is probably the main route involved in pathogenesis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Base Sequence
  • Becaplermin
  • Cell Line
  • Cell Proliferation
  • Collagen Type IV / metabolism*
  • Cytokines / genetics
  • Mesangial Cells / immunology
  • Mesangial Cells / metabolism*
  • Mesangial Cells / pathology*
  • Platelet-Derived Growth Factor / antagonists & inhibitors
  • Platelet-Derived Growth Factor / metabolism
  • Proto-Oncogene Proteins c-sis
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Rats
  • Serpins / genetics*
  • Serpins / metabolism
  • Transfection
  • Transforming Growth Factor beta1 / metabolism
  • Up-Regulation


  • Collagen Type IV
  • Cytokines
  • Platelet-Derived Growth Factor
  • Proto-Oncogene Proteins c-sis
  • RNA, Messenger
  • Serpinb7 protein, rat
  • Serpins
  • Transforming Growth Factor beta1
  • Becaplermin