April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
The Effect Of Intravitreal Rock Inhibitor (H1152p) On Inflammation, RGC Loss And Axonal Regeneration In Experimental Model Of Adult Rodent Anterior Ischemic Optic Neuropathy
Author Affiliations & Notes
  • Masoud A. Fard
    Ophthalmology, Wilmer Eye Institute, Baltimore, Maryland
  • Neil R. Miller
    Ophthalmology, Wilmer Eye Institute, Baltimore, Maryland
  • Katayoon B. Ebrahimi
    Ophthalmology, Wilmer Eye Institute, Baltimore, Maryland
  • Steve L. Bernstein
    Ophthalmology, University of Maryland, Baltimore, Maryland
  • Footnotes
    Commercial Relationships  Masoud A. Fard, None; Neil R. Miller, None; Katayoon B. Ebrahimi, None; Steve L. Bernstein, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 4670. doi:
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      Masoud A. Fard, Neil R. Miller, Katayoon B. Ebrahimi, Steve L. Bernstein; The Effect Of Intravitreal Rock Inhibitor (H1152p) On Inflammation, RGC Loss And Axonal Regeneration In Experimental Model Of Adult Rodent Anterior Ischemic Optic Neuropathy. Invest. Ophthalmol. Vis. Sci. 2011;52(14):4670.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract
 
Purpose:
 

To analyze the outcomes of Rho-kinase (ROCK) inhibition on inflammation,retinal ganglion cell (RGC) survival and axonal regenerationin an experimental model of adult rodent anterior ischemic opticneuropathy.

 
Methods:
 

Anterior ischemic optic neuropathy was induced with a novelphotoembolic mechanism. Immunohistochemistry and Western blotwere performed to detect activation of RhoA signaling and inflammation.Specific ROCK-inhibitor H-1152P was administered intravitreallyone day after ischemia The extent of inflammation, RGC lossand axonal regeneration was determined after 8 and 14 days.

 
Results:
 

After the ischemic event, we observed severe inflammation, RhoAactivity and RGC loss. RGC loss was significantly reduced inresponse to 1µM H-1152P. This was associated with a decreasein the level of inflammatory cells. H-1152P also resulted inaxonal regeneration after optic nerve ischemia.

 
Conclusions:
 

These results demonstrate the neuroprotective effect of H-1152P-mediatedROCK-inhibition on retinal ganglion cells after ischemia.  

  

 
Keywords: neuroprotection • ganglion cells • optic nerve 
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