ScholarWorksIndianapolis
  • Communities & Collections
  • Browse ScholarWorks
  • English
  • Català
  • Čeština
  • Deutsch
  • Español
  • Français
  • Gàidhlig
  • Italiano
  • Latviešu
  • Magyar
  • Nederlands
  • Polski
  • Português
  • Português do Brasil
  • Suomi
  • Svenska
  • Türkçe
  • Tiếng Việt
  • Қазақ
  • বাংলা
  • हिंदी
  • Ελληνικά
  • Yкраї́нська
  • Log In
    or
    New user? Click here to register.Have you forgotten your password?
  1. Home
  2. Browse by Author

Browsing by Author "Zhang, Menglan"

Now showing 1 - 1 of 1
Results Per Page
Sort Options
  • Loading...
    Thumbnail Image
    Item
    High glucose-induced Matrilin-2 expression in mouse mesangial cells was mediated by transforming growth factor beta 1 (TGF-β1)
    (Elsevier, 2016-05) Zhang, Shukun; Zhang, Menglan; Huang, Hong; Zhou, Shiying; Du, Yanshneg; Yi, Xin; Luo, Junming; Department of Health Sciences, School of Health and Rehabilitation Sciences
    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.
About IU Indianapolis ScholarWorks
  • Accessibility
  • Privacy Notice
  • Copyright © 2025 The Trustees of Indiana University