October 1998
Volume 39, Issue 11
Free
Articles  |   October 1998
Extracellular matrix production regulation by TGF-beta in corneal endothelial cells.
T Usui; M Takase; Y Kaji; K Suzuki; K Ishida; T Tsuru; K Miyata; M Kawabata; H Yamashita
Author Affiliations
  • T Usui
    Department of Ophthalmology, Faculty of Medicine, University of Tokyo, Japan.
  • M Takase
    Department of Ophthalmology, Faculty of Medicine, University of Tokyo, Japan.
  • Y Kaji
    Department of Ophthalmology, Faculty of Medicine, University of Tokyo, Japan.
  • K Suzuki
    Department of Ophthalmology, Faculty of Medicine, University of Tokyo, Japan.
  • K Ishida
    Department of Ophthalmology, Faculty of Medicine, University of Tokyo, Japan.
  • T Tsuru
    Department of Ophthalmology, Faculty of Medicine, University of Tokyo, Japan.
  • K Miyata
    Department of Ophthalmology, Faculty of Medicine, University of Tokyo, Japan.
  • M Kawabata
    Department of Ophthalmology, Faculty of Medicine, University of Tokyo, Japan.
  • H Yamashita
    Department of Ophthalmology, Faculty of Medicine, University of Tokyo, Japan.
Investigative Ophthalmology & Visual Science October 1998, Vol.39, 1981-1989. doi:
  • Views
  • PDF
  • Share
  • Tools
    • Alerts
      User Alerts
      You are adding an alert for:
      Extracellular matrix production regulation by TGF-beta in corneal endothelial cells.
      You will receive an email whenever this article is corrected, updated, or cited in the literature. You can manage this and all other alerts in My Account
      The alert will be sent to:
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation
      Citation

      T Usui, M Takase, Y Kaji, K Suzuki, K Ishida, T Tsuru, K Miyata, M Kawabata, H Yamashita; Extracellular matrix production regulation by TGF-beta in corneal endothelial cells.. Invest. Ophthalmol. Vis. Sci. 1998;39(11):1981-1989.

      Download citation file:

      © ARVO (1962-2015); The Authors (2016-present)

      ×
    • Get Permissions
  • Supplements
This content is PDF only. Please click on the PDF icon to access.
Abstract

PURPOSE: Production of extracellular matrix (ECM) by corneal endothelial cells is related to physiologic functions and pathologic conditions and is regulated by many cytokines, including transforming growth factor-beta (TGF-beta). In this study, the molecular mechanism of ECM production regulation by TGF-beta was investigated in cultured corneal endothelial cells. METHODS: The production of ECM components (laminin and fibronectin) was detected in cultured corneal endothelial cells by western blot analysis. To determine the signal transduction pathways, mutant TGF-beta type I receptor (TbetaR-I) and/or Smad protein family members (intracellular signal transducers in TGF-beta signaling) were overexpressed by transfecting their cDNA into the cultured cells, and the effects on ECM production were observed. RESULTS: The production of laminin and fibronectin was stimulated by treatment with TGF-beta1 or TGF-beta2. After transient transfection of cDNA of the constitutively active (CA) mutant of TbetaR-I, the production of laminin and fibronectin was stimulated even in the absence of TGF-beta. The transfection of the dominant negative mutant of TbetaR-I counteracted the effects of TGF-beta. These results confirm that TGF-beta directly stimulates ECM production from corneal endothelial cells through TbetaR-I. The ECM production stimulation by TGF-beta or CA TbetaR-I was accelerated by the overexpression of Smad2, Smad3, and/or Smad4 and inhibited by that of Smad7. These results show that TGF-beta signals connected to ECM production are regulated by Smad family members, located downstream of TbetaR-I. CONCLUSIONS: The results of this study show that TGF-beta stimulates ECM production from corneal endothelial cells through TbetaR-I and Smad family transducers.

Copyright © 2025 Association for Research in Vision and Ophthalmology.
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×
This site uses cookies. By continuing to use our website, you are agreeing to our privacy policy.Accept