English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

. Smad7, a protein induced by transforming growth factor–β1 (TGF-β1) in many target cells, inhibits TGF-β1 signal transduction and is thought to mediate an intracellular negative feedback response that limits TGF-β1 effects. It is possible that overexpression of Smad7 could block specified effects of TGF-β1 on mesangial cells, a TGF-β target in glomerular disease. Smad7 mRNA was induced by TGF-β1 within 1 h in a concentration-dependent manner in a transformed mouse mesangial cell (MMC) line. Uptake of  14 C-spermidine from the medium by MMC and the transcriptional activity of a segment of the human collagen pro-α2 type 1 chain ( COL1A2 ) promoter fused to a luciferase reporter gene were used as indices of TGF-β1. Treatment with TGF-β1 increased  14 C-spermidine uptake rate in a time-, concentration-, and temperature-dependent manner. For example, exposure to 1 ng/ml TGF-β1 for 15 h increased uptake approximately twofold, a response that was attenuated by cycloheximide. Transfection of Smad7 expression vector into MMC abrogated both TGF-β1-dependent stimulation of spermidine uptake and  COL1A2  promoter activity. It is concluded that: ( 1 ) TGF-β1 induces Smad7 in MMC; ( 2 )  14 C-spermidine uptake is a convenient quantitative index of TGF-β1 effect in these cells; and ( 3 ) overexpression of Smad7 is a highly effective method of blocking at least some mesangial cell effects of TGF-β1 that may warrant evaluation  in vivo  in experimental glomerular disease.

Blockade of the Effects of TGF-β1 on Mesangial Cells by Overexpression of Smad7