April 2009
Volume 50, Issue 13
ARVO Annual Meeting Abstract  |   April 2009
Effect of EGF-induced Deacetylation on Corneal Epithelial Wound Healing
Author Affiliations & Notes
  • L. Lu
    Medicine, David Geffen Sch of Med/UCLA, Torrance, California
  • Footnotes
    Commercial Relationships  L. Lu, None.
  • Footnotes
    Support  NIH EY15281
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 6295. doi:
  • Views
  • Share
  • Tools
    • Alerts
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      L. Lu; Effect of EGF-induced Deacetylation on Corneal Epithelial Wound Healing. Invest. Ophthalmol. Vis. Sci. 2009;50(13):6295.

      Download citation file:

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

  • Supplements

Purpose: : Epidermal Growth factor (EGF) plays important roles in regulating corneal epithelial proliferation/differentiation during wound healing. The purpose of the study is to investigate effects of EGF-induced deacetylation on corneal epithelial migration and wound healing.

Methods: : Human and rabbit corneal epithelial cells (HCE and RCE cells) were cultured in DMEM/F12 medium contained 10% FBS in 37 °C incubator supplied with 5% CO2. Northern blot and Western analysis were used to determine target gene and protein expressions. Activity of HDAC6 was suppressed by trichostatin A (TSA) and by siRNA specific to HDAC6 mRNA. Corneal epithelial cell proliferation was measured by corneal epithelial migration and debridement wound healing model.

Results: : We found EGF-stimulated corneal epithelial cell migration and wound healing through enhancing HDAC6 activity and deacetylation of -tubulin. We report in the study: 1) EGF induced an increase in HDAC6 activity and enhanced decetylation of -tubulin; 2) EGF-induced HCE cell migration was suppressed by TSA-induced inhibition of HDAC6 activity; 3) knockdown of HDAC6 mRNA with specific siRNA effectively abolished EGF-induced deacetylation of -tubulin and significantly inhibited HCE cell migration; 4) inhibition of Erk signaling pathway with PD98059 suppressed EGF-induced HDAC6 activation; and 5) suppression of HDAC6 activity with TSA significantly delayed EGF-induced wound healing in epithelial debrided corneas.

Keywords: cornea: epithelium • growth factors/growth factor receptors • wound healing 

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.