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

Authors: Xia, Y  Zhang, Y  Shi, W  Liu, S  Chen, Y  Liang, X  Ye, Z 
Citation: Xia Y, etal., Cell Immunol. 2011;271(2):413-7. doi: 10.1016/j.cellimm.2011.08.009. Epub 2011 Sep 5.
Pubmed: (View Article at PubMed) PMID:21945418
DOI: Full-text: DOI:10.1016/j.cellimm.2011.08.009

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-beta1 upregulation. Concentrations of PDGF-BB, TGF-beta1 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-beta1 in stable transformant MCs, suggesting that over-expression of megsin induces cell proliferation and ECM accumulation in MCs, upregulation of PDGF-BB and TGF-beta1 is probably the main route involved in pathogenesis.

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CRRD Object Information
CRRD ID: 7207383
Created: 2013-01-30
Species: All species
Last Modified: 2013-01-30
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.