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Ryo Terauchi, Tsutomu Sakai, Tadashi Nakano, Hideo Kohno; Minocycline suppresses microglial Ccr2 expression in inherited retinal degeneration. Invest. Ophthalmol. Vis. Sci. 2019;60(9):432.
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© ARVO (1962-2015); The Authors (2016-present)
Excessive retinal inflammation accelerates photoreceptor cell death (PCD) in retinal degenerative diseases (RDDs). We previously reported that Ccr2 positive microglial cells play dominant role in retinal inflammation which accelerate PCD. Minocycline, a broad-spectrum tetracycline antibiotic, modulates microglial activation, is expected as potential inflammation-targeted treatment candidate for RDDs. In this study, we investigated whether minocycline had an impact on microglial Ccr2 expression in mouse model of inherited retinal degeneration.
Mertk-/-Cx3cr1GFP/-Ccr2RFP/- mice received once-daily intraperitoneal injections of minocycline at a dose of 50 mg/kg (Mino50), 100 mg/kg (Mino100), or PBS as control, starting from postnatal day 28 (P28) and continuing through to P42. Slide-mounted sections of eyes at P42 were observed using a confocal microscopy.
Mino50 and Mino100 showed significantly reduced Ccr2 positive cells compared to PBS in flatmounts of retina (P < .001, .001) and retinal pigment epithelium (RPE) (P = .030, < .001). On the contrary, minocycline had no impact on the number of Cx3cr1 positive cells.
The suppression of microglial Ccr2 expression is the one of mechanism of anti-retinal inflammatory effect by minocycline.
This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.
Cx3cr1-GFP and Ccr2-RFP dual positive activated microglia observed in the outer retina.
Cx3cr1-GFP and Ccr2-RFP positive cells in retina flatmounts of control, Mino50 or Mino100.
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