December 2002
Volume 43, Issue 13
Free
ARVO Annual Meeting Abstract  |   December 2002
Brimonidine induces the expression of ELAM-1 in TM cells
Author Affiliations & Notes
  • S Diskin
    New England Eye Center Tufts University School of Medicine Tufts Sackler School of Graduate Biomedical Sciences and Tufts Center for Vision Research Boston MA
  • N Wang
    New England Eye Center Tufts University School of Medicine Tufts Sackler School of Graduate Biomedical Sciences and Tufts Center for Vision Research Boston MA
  • ME Fini
    New England Eye Center Tufts University School of Medicine Tufts Sackler School of Graduate Biomedical Sciences and Tufts Center for Vision Research Boston MA
  • JS Schuman
    New England Eye Center Tufts University School of Medicine Tufts Sackler School of Graduate Biomedical Sciences and Tufts Center for Vision Research Boston MA
  • Footnotes
    Commercial Relationships   S. Diskin, None; N. Wang, None; M.E. Fini, None; J.S. Schuman, Allergan F, R. Grant Identification: RO1-EY13178, R01-EY09828, P30-EY13078,Lions Eye Research Fund, Inc.,Research To Prevent Blindness
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 4103. doi:
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    • Get Citation

      S Diskin, N Wang, ME Fini, JS Schuman; Brimonidine induces the expression of ELAM-1 in TM cells . Invest. Ophthalmol. Vis. Sci. 2002;43(13):4103.

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Abstract

Abstract: : Purpose: A study conducted in our lab (Nat. Med. Vol. 7 No.3 March 2001) has identified Endothelial Leukocyte Adhesion Molecule-1 (ELAM-1) as a molecular marker for glaucomatous trabecular meshwork (TM). Its expression is due to the activation of the NF-kB/IL-1 signal transduction pathway. The activation of the ELAM-1/NF-kB/IL-1 pathway protects TM cells from oxidative stress in culture. Brimonidine is an adrenergic agonist that reduces the formation of aqueous humor in the eye. It has also recently been shown to be neuroprotective. The purpose of the current study is to learn whether brimonidine might also be protective of TM cells through induction the ELAM-1/NF-kB/IL-1 pathway. Methods: Early passage TM cells derived from normal or glaucomatous eyes were plated to 4-chamber slides. The cells were than exposed to varying concentrations of brimonidine diluted in Dulbecco’s Modified Eagle’s Medium without serum. The cells were incubated with the drug for periods of 1, 4, 8 or 24 hrs. Cells on each slide were then fixed and subjected to immunostaining with a mouse anti-human ELAM-1 antibody. Results: Untreated TM cells from normal eyes did not express ELAM-1. In contrast, normal TM cells treated with brimonidine expressed ELAM-1 in a dose-dependent manner. A concentration of 10(-6)M brimonidine induced expression of ELAM-1 in 42% of cells, while a concentration of 10(-5)M induced expression in 82% of the cells. TM cells from glaucomatous eyes expressed ELAM-1 constitutively, but the pattern of expression in brimonidine-treated cells seemed to change, shifting from a peripheral to a more peri-nuclear localization pattern. Conclusion: Our data are consistent with the hypothesis that brimonidine induces the ELAM-1/NF-kB/IL-1 pathway. This suggests that brimonidine may protect TM cells against stress.

Keywords: 581 signal transduction: pharmacology/physiology • 601 trabecular meshwork • 592 stress response 
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