June 2017
Volume 58, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2017
Targeting plasma membrane repair in corneal wound healing
Author Affiliations & Notes
  • Heather L Chandler
    The Ohio State University, Columbus, Ohio, United States
  • Rita Fay Wehrman
    Iowa State University, Ames, Iowa, United States
  • Anne J Gemensky-Metzler
    The Ohio State University, Columbus, Ohio, United States
  • Footnotes
    Commercial Relationships   Heather Chandler, None; Rita Wehrman, None; Anne Gemensky-Metzler, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science June 2017, Vol.58, 3376. doi:
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      Heather L Chandler, Rita Fay Wehrman, Anne J Gemensky-Metzler; Targeting plasma membrane repair in corneal wound healing. Invest. Ophthalmol. Vis. Sci. 2017;58(8):3376.

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

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Purpose : To evaluate the protective role that MG53, an essential gene for cell membrane repair, plays in corneal wound healing.

Methods : Western blots were used to determine MG53 expression in human corneal epithelial cells (hCEC), human tears, and canine aqueous humor. Membrane repair was evaluated using microelectrode penetration in GFP-MG53 expressing hCEC with subsequent observation of translocation. Additionally, hCEC and canine stromal fibroblasts underwent micro-glass bead damage followed by treatment with recombinant human (rh)MG53 and viability analysis. The effects on corneal wound healing were evaluated using an in vitro scratch model and an in vivo rat injury model.

Results : hCEC, tears, and aqueous humor express MG53 and live cell imaging revealed that extracellular rhMG53 can enter normal hCEC and stromal fibroblasts via receptor mediated endocytosis. Cell damage induced via microelectrode penetration stimulated nucleation of GFP-MG53 to injury sites in hCEC. Application of rhMG53 significantly (p<0.01) improved hCEC and stromal fibroblast viability against mechanical injury induced by micro-glass beads. rhMG53 enhanced in vitro and in vivo wound healing by stimulating re-epithelialization and promoting the migration of corneal fibroblasts, but not corneal myofibroblasts.

Conclusions : Expression of MG53 in hCEC, human tears, and canine aqueous humor indicates that MG53 may be an intrinsic protective factor in the cornea in multiple species. Moreover, MG53 can play an important role in corneal wound healing by enhancing hCEC membrane repair and restoration of the ocular surface.

This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.


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