June 2015
Volume 56, Issue 7
ARVO Annual Meeting Abstract  |   June 2015
Role of Focal Adhesion Kinase (FAK) in RGC in Glaucoma
Author Affiliations & Notes
  • M Livia Bajenaru
    Miller School of Medicine, Univ of Miami, Bascom Palmer Eye Inst, Miami, FL
  • Andrea Rachelle C Santos
    Miller School of Medicine, Univ of Miami, Bascom Palmer Eye Inst, Miami, FL
  • Kevin K Park
    The Miami Project to Cure Paralysis, Miller School of Medicine, Univ of Miami, Miami, FL
  • Sander R Dubovy
    Miller School of Medicine, Univ of Miami, Bascom Palmer Eye Inst, Miami, FL
  • Antonio Bermudez
    Miller School of Medicine, Univ of Miami, Bascom Palmer Eye Inst, Miami, FL
  • Footnotes
    Commercial Relationships M Livia Bajenaru, None; Andrea Santos, None; Kevin Park, None; Sander Dubovy, None; Antonio Bermudez, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 2445. doi:
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      M Livia Bajenaru, Andrea Rachelle C Santos, Kevin K Park, Sander R Dubovy, Antonio Bermudez; Role of Focal Adhesion Kinase (FAK) in RGC in Glaucoma. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):2445.

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

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Purpose: Extensive remodeling of extracellular matrix (ECM) and changes in the expression of integrins are typical to glaucoma and associated with RGC death and degeneration. We recently showed that laminin-integrin-FAK-Akt pathway is disrupted in retinal ischemia. The purpose of this study is to investigate the role of FAK in RGC in glaucoma.

Methods: Experimental glaucoma was induced in the left eye of 30 Sprague Dawley rats by blocking the ocular outflow and producing increased intraocular pressure (IOP) using a diode laser. IOP was measured periodically in both eyes after laser photocoagulation (LP). A group of rats (n=8) was euthanized 9 weeks post LP. Their optic nerves and retinas were removed and processed for histology. Semi-automated counting of the axons was performed in optic nerve cross sections stained with toluidine blue. Corresponding flat mounted retinas were processed for immunofluorescence with a TUJ1 (βIII tubulin) antibody, and TUJ1 labeled RGC were counted with an inverted fluorescence microscope. Another group of rats (n=8) was euthanized 4 weeks post-LP and fluorogold (FG) labeled RGC were counted in flat mounted retinas. Retinal flat-mounts (n=4) from control and experimental glaucoma eyes 2 weeks post-LP, and human normal (n=2) and glaucomatous (n=4) retinas and optic nerves were processed for immunohistochemsitry with β1-integrin, FAK, phospho-FAK antibodies

Results: Mean IOP was increased in the treated eye from 8.66±1.03 to 18.34±5.86 to a peak value of 25.73± 9.73 at 1 day, 16.44 ± 6.98 at 1, and 20.75 ± 7.27 mm Hg at 2 weeks post LP (*p<0.05). Axonal loss at 9 weeks post-LP, was 64.89% ± 11.05 (*p<0.05), in good correlation with RGC survival, 52.39% ± 4.74 (*p<0.01),Loss of FG labeled RGCs was aparent at 2 weeks, with significantly reduced FG+ RGCs in the glaucomatous eye at 4 weeks post LP (12.66% ± 9.21; *p<0.05), suggesting that many surviving RGCs are dysfunctional and have impaired retrograde active transport. Toluidine blue staining in optic nerve cross-sections showed swollen axons, collapsed myelin sheets, and axon bundles disarray 9 weeks post-LP in treated eyes. Immunohistochemistry showed decreased expression of β1-integrin and significantly reduced phospho/activated FAK in both human and experimental glaucoma.

Conclusions: Our results suggest that β1 integrin signaling is disrupted with significantly reduced FAK activation in RGC in glaucoma.


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