High glucose-induced Matrilin-2 expression in mouse mesangial cells was mediated by transforming growth factor beta 1 (TGF-β1)
dc.contributor.author | Zhang, Shukun | |
dc.contributor.author | Zhang, Menglan | |
dc.contributor.author | Huang, Hong | |
dc.contributor.author | Zhou, Shiying | |
dc.contributor.author | Du, Yanshneg | |
dc.contributor.author | Yi, Xin | |
dc.contributor.author | Luo, Junming | |
dc.contributor.department | Department of Health Sciences, School of Health and Rehabilitation Sciences | en_US |
dc.date.accessioned | 2016-12-09T21:07:54Z | |
dc.date.available | 2016-12-09T21:07:54Z | |
dc.date.issued | 2016-05 | |
dc.description.abstract | 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-β1) inhibitors and TGF-β1 were used to determine whether glucose-regulated Matrilin-2 expression was mediated by the TGF-β1/Smad3 signaling pathway. Our data demonstrated that Matrilin-2 expression was markedly induced by high glucose and TGF-β1. High glucose-induced Matrilin-2 expression was inhibited by TGF-β1/Smad3 inhibitors, indicating that Matrilin-2 was markedly induced by high glucose and this induction was mediated by the TGF-β1/Smad3 pathway. Taken together, our results showed that high-glucose-induced Matrilin-2 expression that was mediated by the TGF-β1/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. | en_US |
dc.eprint.version | Author's manuscript | en_US |
dc.identifier.citation | Zhang, S., Zhang, M., Huang, H., Zhou, S., Du, Y., Yi, X., & Luo, J. (2016). High glucose-induced Matrilin-2 expression in mouse mesangial cells was mediated by transforming growth factor beta 1 (TGF-β1). Biochemical and Biophysical Research Communications, 474(2), 303–308. https://doi.org/10.1016/j.bbrc.2016.04.091 | en_US |
dc.identifier.uri | https://hdl.handle.net/1805/11606 | |
dc.language.iso | en | en_US |
dc.publisher | Elsevier | en_US |
dc.relation.isversionof | 10.1016/j.bbrc.2016.04.091 | en_US |
dc.relation.journal | Biochemical and Biophysical Research Communications | en_US |
dc.rights | IUPUI Open Access Policy | en_US |
dc.source | Author | en_US |
dc.subject | diabetic nephropathy | en_US |
dc.subject | extracellular matrix | en_US |
dc.subject | Matrilin-2 | en_US |
dc.title | High glucose-induced Matrilin-2 expression in mouse mesangial cells was mediated by transforming growth factor beta 1 (TGF-β1) | en_US |
dc.type | Article | en_US |