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S. Morales, M. Wadehra, J. Braun, L. Gordon; Pro–Inflammatory Stimuli Alters Epithelial Membrane Protein 2 (EMP2) Expression in Retinal Pigment Epithelium . Invest. Ophthalmol. Vis. Sci. 2005;46(13):3060.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose:Multiple inflammatory cytokines, including IL–1 α and TNF–α, induce a biologic response in retinal pigment epithelium (RPE) including upregulation of TNF receptor, enhanced secretion of matrix metalloproteinases (MMP), and increased RPE cell adhesion and migration. These changes are relevant to control of the ocular microenvironment during intraocular inflammation and in the aberrant wound healing response of proliferative vitreoretinpathy (PVR). Control of cell surface expression of specific integrin isoforms, which influence extracellular matrix interactions, is linked to the expression of epithelial membrane protein 2 (EMP2). The promoter of EMP2, a four transmembrane protein, contains putative inflammatory response elements. The purpose of this project is to investigate whether, IL–1α and TNF–α, can influence RPE cell biology through increasing EMP2 expression. Methods: ARPE–19, a human cell line derived from retinal pigment epithelium, was obtained from ATCC. Immunologic methods, including immunofluorescence and Western blot, as well as RT–PCR confirmed a high level of EMP2 expression in ARPE–19. Modulation of EMP2 protein expression was achieved with a 48hr treatment of IL–1α (1–20ng/ml) and TNF–α (1–20ng/ml). EMP2 expression was quantified using Western blot. Results:ARPE–19 cells treated with IL–1α and TNF–α increase EMP2 protein expression when compared to untreated cells. TNF–α induced an eight–fold increase in EMP2 expression as compared to controls. IL–1α induced a two–fold increase in EMP2 expressionn EMP2 expression as compared to controls.. In both cases, a dose–response relationship was observed with a peak response at 10ng/ml. Conclusions:Pro–inflammatory stimuli, IL–1α and TNF–α, increase expression of EMP2 in ARPE–19 cells. Since EMP2 regulates surface expression of integrin isoforms, this finding provides a specific biochemical link between inflammation and RPE traits involved in PVR.
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