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Yang Liu, Jessica Manheim, Shaohua Yang, Robert J Wordinger, Abbot F Clark, Iok-Hou Pang; Glial cell specific deletion of p38 MAPK did not affect retinal ganglion cell degeneration following optic nerve crush. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):4949.
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© ARVO (1962-2015); The Authors (2016-present)
Reactive gliosis affects retinal ganglion cell (RGC) degeneration under stress conditions. p38 mitogen-activated protein kinase (p38K) is a major stress-activated signaling pathway. In this study, we evaluated the effects of glia-specific knockout of p38K on RGC degeneration induced by optic nerve crush (ONC).
Mice with LoxP sites flanking the p38K gene were crossed to mice expressing GFAP-CRE to generate mice lacking p38K in glial cells. Intraorbital ONC was performed. Following optic nerve injury, RGC survival was determined by RNA-binding protein with multiple splicing (RBPMS) immunofluorescence staining of retinal flat mounts. Expression and location of proteins were evaluated by immunohistochemistry in retinal cross-sections. Retinal function was assessed by analysis of amplitude of positive scotopic threshold response (pSTR) of full field flash electroretinography (ERG).
Intraorbital ONC increased levels of phosphorylated p38K in astroglial cells in the mouse optic nerve. ONC induced significant RGC loss 7 days after the injury in retinas of both glia-specific p38K knockout mice and their littermate controls (n=5, p<0.05). The deletion of p38K in glial cells did not affect the numbers of remaining RGCs after ONC (n=5, p>0.05). ERG analysis also showed similar reduction of pSTR amplitudes in p38K knockout mice compared to their littermate controls (n=5, p>0.05).
Deletion of p38K in glial cells did not affect RGC degeneration following optic nerve injury. Under the current study conditions, p38K does not appear to be a major pathway involved in RGC degeneration or survival.
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