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A.B. D. Collins, B.D. Korman, C. Yu, X. Liu, R.M. Mahdi, R.A. Bush, X. Ma, C.E. Egwuagu, I. Gery; Anti–Inflammatory Molecules, GC–BP and TREM2, are Constitutively Expressed in the Mouse Eye . Invest. Ophthalmol. Vis. Sci. 2006;47(13):1778.
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© ARVO (1962-2015); The Authors (2016-present)
Inflammation is detrimental to ocular tissues and several mechanisms have been found to protect the eye against inflammation. Recent studies have identified two molecules that inhibit inflammation, namely, Triggering Receptor Expressed on Myeloid Cells 2 (TREM2) ( J. Exp. Med., 2005, 201:647), and GC–binding protein (GC–BP) (Immunity, 2004, 21:643). This study was aimed at examining the expression of these two molecules in the normal mouse retina, as well as, in retinas damaged by inflammation or exposure to bright light.
For induction of experimental autoimmune uveitis (EAU), B10.RIII mice were immunized with IRBP peptide p161–180 in CFA. Clinical and histological changes were evaluated 7, 14 and 28 days post–immunization. Light damage was induced in BALB/C mice by exposure to 5000 lux white light for 8 or 25 hours, which induces apoptosis in a large number of photoreceptors. Retinas from the experimental mice and their untreated controls were isolated immediately after euthanasia and RNA or protein were extracted by conventional methods. RNA samples were examined for transcripts of TREM2 and GC–BP by RT–PCR and real time PCR procedures, while the presence of the two proteins was detected by Western blotting.
RT–PCR and Western blot analysis revealed that both GC–BP and TREM2 are expressed in the mouse retina. Initial signs of EAU were observed 10 days post–immunization, with peak EAU at day 14 and subsequent disease resolution by day 28 post–immunization. We detected the same levels of GC–BP protein in control, uveitic, as well as, light damaged eyes. In contrast, low levels of TREM2 were detected in the retina of control mice and at day 7 post–immunization with IRBP peptide, but the level increased on day 14, coinciding with peak of disease. On the other hand we observed a decrease in expression of TREM2 in retinas damaged by white light.
We provide evidence for the first time that GC–BP and TREM2 proteins are constitutively expressed in the retina. Although TREM2 expression is relatively low in the normal mouse retina, its level increases considerably during inflammation. The increase in TREM2 during inflammation suggests a potential role of this protein in protecting the neural retina from cytotoxic effects of proinflammatory cytokines.
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