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Yoko Okunuki, Eiichi Hasegawa, Ryo Mukai, Clifford Kim, Garrett Klokman, Saori Inafuku, Kip M Connor; The role of microglial expression of microRNA-155 on a murine model of retinal detachment. Invest. Ophthalmol. Vis. Sci. 2016;57(12):5379.
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© ARVO (1962-2015); The Authors (2016-present)
Retinal detachment (RD) is a sight threatening disorder characterized by the physical separation of the photoreceptors from the retinal pigment epithelium. As a result, the detached photoreceptors undergo apoptosis and programmed cell death. It has been reported that retinal microglia become activated during RD however, the role of microglia in the pathophysiology of photoreceptor cell death is not well understood. The association of pro-inflammatory microRNA-155 (miR-155), abundantly expressed in microglia, is suggested to be associated with worsening of neurodegenerative brain diseases. In this study, we examined the role of miR-155 on photoreceptor cell death in RD.
RD was induced by subretinal injection of 4 ul of sodium hyaluronate in miR-155 -/- mice and C57BL/6J mice. Microglia were isolated from intact retinas and 24hr post RD retinas of C57BL/6J mice by fluorescence-activated cell sorting, and miR-155 expression in microglia was measured by RT-PCR. RD-induced photoreceptor cell death was compared between miR-155 -/- mice and C57BL/6J mice by TUNEL staining.
MiR-155 expression in microglia was significantly increased in 24hr post RD retinas compared to intact retinas (p<0.001). The number of TUNEL positive cells in miR-155 -/- retinas was significantly decreased 24hrs after RD (p=0.008, n=8).
We demonstrated that miR-155 expression in microglia was increased after RD in mice. Systemic defect of miR-155 suppressed photoreceptor cell death caused by RD. These results suggest that miR-155 defect protects photoreceptor cells from cell death, although the exact role of microglial expression of miR-155 with retinal damage still needs to be explored.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.
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