Store-operated calcium entry suppressed the TGF-β1/Smad3 signaling pathway in glomerular mesangial cells.

ABSTRACT: Our previous study demonstrated that the abundance of extracellular matrix proteins was suppressed by store-operated Ca²⁺ entry (SOCE) in mesangial cells (MCs). The present study was conducted to investigate the underlying mechanism focused on the transforming growth factor-β1 (TGF-β1)/Smad3 pathway, a critical pathway for ECM expansion in diabetic kidneys. We hypothesized that SOCE suppressed ECM protein expression by inhibiting this pathway in MCs. In cultured human MCs, we observed that TGF-β1 (5 ng/ml for 15 h) significantly increased Smad3 phosphorylation, as evaluated by immunoblot. However, this response was markedly inhibited by thapsigargin (1 µM), a classical activator of store-operated Ca²⁺ channels. Consistently, both immunocytochemistry and immunoblot sho

SUBMITTER: Chaudhari S 

PROVIDER: S-EPMC5625109 | biostudies-literature | 2017 Sep

REPOSITORIES: biostudies-literature