| First Author | Zhang S | Year | 2016 |
| Journal | Biochem Biophys Res Commun | Volume | 474 |
| Issue | 2 | Pages | 303-308 |
| PubMed ID | 27105914 | Mgi Jnum | J:235163 |
| Mgi Id | MGI:5793004 | Doi | 10.1016/j.bbrc.2016.04.091 |
| Citation | Zhang S, et al. (2016) High glucose-induced Matrilin-2 expression in mouse mesangial cells was mediated by transforming growth factor beta 1 (TGF-beta1). Biochem Biophys Res Commun 474(2):303-8 |
| abstractText | This study aimed at evaluating the effect of high glucose on the expression of extracellular matrix (ECM) protein Matrilin-2 and the mechanism underlying this effect by using a mouse mesangial cell line. Mouse mesangial cells (MMCs) were cultured in media containing normal (5 mM d-glucose) or high concentrations of glucose (30 mM d-glucose). The expression of Matrilin-2 was assessed by either RT-PCR or western blot. Additionally, transforming growth factor beta 1 (TGF-beta1) inhibitors and TGF-beta1 were used to determine whether glucose-regulated Matrilin-2 expression was mediated by the TGF-beta1/Smad3 signaling pathway. Our data demonstrated that Matrilin-2 expression was markedly induced by high glucose and TGF-beta1. High glucose-induced Matrilin-2 expression was inhibited by TGF-beta1/Smad3 inhibitors, indicating that Matrilin-2 was markedly induced by high glucose and this induction was mediated by the TGF-beta1/Smad3 pathway. Taken together, our results showed that high-glucose-induced Matrilin-2 expression that was mediated by the TGF-beta1/Smad3 signaling pathway might play a role in Diabetic nephropathy (DN) pathogenesis and our finding provided a potential diagnostic and/or therapeutic target for DN. |
