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Abstract #58726 Published in IGR 16-3
Fractalkine receptor regulates microglial neurotoxicity in an experimental mouse glaucoma model
Wang K; Peng B; Lin BGLIA 2014; 62: 1943-1954
Neuroinflammation underlies a wide variety of pathological processes in the central nerve system (CNS). Although previous experimental and clinical studies indicate that activation of neuroinflammatory signaling occurs early in glaucoma, the mechanisms controlling microglia activation are still poorly defined. In the present study, we investigated the role of the chemokine receptor Cx3cr1 in microglia activation and retinal ganglion cell (RGC) death in an experimental mouse glaucoma model with transient elevation of intraocular pressure (IOP). We demonstrated that retinal microglia played a pathogenic role in RGC death. Conversely, pharmacological suppression of microglia activation by minocycline increased RGC survival. Moreover, we found that Cx3cr1 deficiency enhanced microglial neurotoxicity and subsequently induced more extensive RGC loss, suggesting that Cx3cr1 suppressed microglial activation under elevated IOP. Overall, these findings provided novel insight into the mechanisms by which Cx3cr1 modulated microglia activation under elevated IOP. Suppression of microglia activation might be a potential treatment for slowing down the course of the disease and for increasing RGC survival in glaucoma patients.
Department of Anatomy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong.
Full articleClassification:
5.1 Rodent (Part of: 5 Experimental glaucoma; animal models)
11.8 Neuroprotection (Part of: 11 Medical treatment)
3.10 Immunobiology (Part of: 3 Laboratory methods)
