March 1992
Volume 33, Issue 3
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Articles  |   March 1992
Identification and partial characterization of TGF-beta 1 receptors on trabecular cells.
Author Affiliations
  • N S Borisuth
    Department of Ophthalmology and Visual Science, University of Chicago, Illinois 60637.
  • B J Tripathi
    Department of Ophthalmology and Visual Science, University of Chicago, Illinois 60637.
  • R C Tripathi
    Department of Ophthalmology and Visual Science, University of Chicago, Illinois 60637.
Investigative Ophthalmology & Visual Science March 1992, Vol.33, 596-603. doi:
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      N S Borisuth, B J Tripathi, R C Tripathi; Identification and partial characterization of TGF-beta 1 receptors on trabecular cells.. Invest. Ophthalmol. Vis. Sci. 1992;33(3):596-603.

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

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Abstract

By using two specific receptor assays, we identified and partially characterized receptors for transforming growth factor-beta 1 (TGF-beta 1) on porcine trabecular cells in vitro. Cultured trabecular cells were incubated with labeled TGF-beta 1 and analyzed by flow cytometry. Pretreatment with trypsin or preincubation with cold TGF-beta 1 or a neutralizing antibody to TGF-beta 1 inhibited the binding of labeled TGF-beta 1. 125I-TGF-beta 1 was cross-linked covalently to cell surface receptors on the trabecular cells. By SDS-PAGE and autoradiography, we identified three labeled macromolecular species of receptors, two of which had apparent molecular weights greater than 212 kDa and one of which had an apparent molecular weight of approximately 80-90 kDa under reducing conditions. The low and high molecular weight species probably represent type II and type III TGF-beta 1 receptors, respectively. At concentrations of 0.5 and 1 ng/ml, activated TGF-beta 1 caused retraction and a marked decrease in the rate of proliferation and in the motility of trabecular cells in vitro. Our findings implicate TGF-beta 1 in the modulation of the functional homeostasis of trabecular cells and suggest that the aqueous humor contains a level of TGF-beta 1 which, once activated, is sufficient to exert a biologic effect on the trabecular meshwork.

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