May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
Upregulation of Fibronectin EDA in RPE Cells by Transforming Growth Factor Beta (TGF-b)
Author Affiliations & Notes
  • R.R. Khankan
    Pathology, Doheny Eye Institute Keck Sch Med U Southern Calif, Los Angeles, CA, United States
  • C. Spee
    Ophthalmology, Doheny Eye Institute Keck Sch Med U Southern Calif, Los Angeles, CA, United States
  • S. He
    Ophthalmology, Doheny Eye Institute Keck Sch Med U Southern Calif, Los Angeles, CA, United States
  • S.J. Ryan
    Ophthalmology, Doheny Eye Institute Keck Sch Med U Southern Calif, Los Angeles, CA, United States
  • D.R. Hinton
    Ophthalmology, Doheny Eye Institute Keck Sch Med U Southern Calif, Los Angeles, CA, United States
  • Footnotes
    Commercial Relationships  R.R. Khankan, None; C. Spee, None; S. He, None; S.J. Ryan, None; D.R. Hinton, None.
  • Footnotes
    Support  NIH grants EY03040 & EY01545; Research to Prevent Blindness; the Arnold & Mabel Beckman Foundation.
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 376. doi:
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      R.R. Khankan, C. Spee, S. He, S.J. Ryan, D.R. Hinton; Upregulation of Fibronectin EDA in RPE Cells by Transforming Growth Factor Beta (TGF-b) . Invest. Ophthalmol. Vis. Sci. 2003;44(13):376.

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

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Abstract

Abstract: : Purpose: One of the earliest extracellular matrix (ECM) components expressed by RPE cells in response to injury is an alternatively spliced embryonic isoform of fibronectin, FN EDA. The purpose of this study was to determine the time and dose response effect of TGF-ß on FN EDA expression. Methods: Human fetal RPE cell cultures (passages 2-4) were exposed to increasing concentrations of both TGF-ß1 and TGF-ß2. FN EDA expression was analyzed at different time points in both cell supernatant and homogenates. Western blot and immunohistochemical analyses were performed utilizing a FN EDA-specific monoclonal antibody. Results: TGF-ß stimulation of RPE cells resulted in a marked dose-dependent increase in FN EDA that increased further with longer exposure to TGF-ß. Results were similar for both TGF-ßs. Conclusions: TGF-ß stimulates expression of FN EDA in RPE. Since TGF-ß is increased in a variety of ocular disorders, this result provides a mechanism by which TGF-ß may contribute to disease pathogenesis with an accumulation of ECM.

Keywords: retinal pigment epithelium • growth factors/growth factor receptors • eye movements 
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