June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Glial cell specific deletion of p38 MAPK did not affect retinal ganglion cell degeneration following optic nerve crush
Author Affiliations & Notes
  • Yang Liu
    Pharmaceutical Sciences, UNT Health Science Center, Fort Worth, TX
    North Texas Eye Research Institute, Fort Worth, TX
  • Jessica Manheim
    Cell Biology and Immunology, UNT Health Science Center, Fort Worth, TX
    North Texas Eye Research Institute, Fort Worth, TX
  • Shaohua Yang
    Department of Pharmacology and Neuroscience, UNT Health Science Center, Fort Worth, TX
  • Robert J Wordinger
    Cell Biology and Immunology, UNT Health Science Center, Fort Worth, TX
    North Texas Eye Research Institute, Fort Worth, TX
  • Abbot F Clark
    Cell Biology and Immunology, UNT Health Science Center, Fort Worth, TX
    North Texas Eye Research Institute, Fort Worth, TX
  • Iok-Hou Pang
    Pharmaceutical Sciences, UNT Health Science Center, Fort Worth, TX
    North Texas Eye Research Institute, Fort Worth, TX
  • Footnotes
    Commercial Relationships Yang Liu, None; Jessica Manheim, None; Shaohua Yang, None; Robert Wordinger, None; Abbot Clark, Genzyme-Sonofi (C), ISIS Pharmaceuticals (C), Reata Pharmaceutical (F), Sanofi-Fovea (C); Iok-Hou Pang, Alcon (C), Novartis (C), Regeneron (C)
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 4949. doi:
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    • Get Citation

      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)

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Abstract

Purpose: 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).

Methods: 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).

Results: 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).

Conclusions: 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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