September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Subbasal Axon Density is Reduced and Reinnervation After Injury Delayed in the Syndecan-1 Null Mouse Cornea.
Author Affiliations & Notes
  • Mary Ann Stepp
    Anatomy and Regenerative Biology, George Washington University, Washington, District of Columbia, United States
  • Gauri Tadvalkar
    Anatomy and Regenerative Biology, George Washington University, Washington, District of Columbia, United States
  • Raymond Hakh
    Anatomy and Regenerative Biology, George Washington University, Washington, District of Columbia, United States
  • Sonali Pal-Ghosh
    Anatomy and Regenerative Biology, George Washington University, Washington, District of Columbia, United States
  • Footnotes
    Commercial Relationships   Mary Ann Stepp, None; Gauri Tadvalkar, None; Raymond Hakh, None; Sonali Pal-Ghosh, None
  • Footnotes
    Support  EY08512, EY021784, and EY023106
Investigative Ophthalmology & Visual Science September 2016, Vol.57, 1292. doi:
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      Mary Ann Stepp, Gauri Tadvalkar, Raymond Hakh, Sonali Pal-Ghosh; Subbasal Axon Density is Reduced and Reinnervation After Injury Delayed in the Syndecan-1 Null Mouse Cornea.. Invest. Ophthalmol. Vis. Sci. 2016;57(12):1292.

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      © 2017 Association for Research in Vision and Ophthalmology.

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Abstract

Purpose : The heparan sulfate proteoglycan syndecan is required for proper growth cone formation in C. elegans; although syndecan-1 is upregulated in wounded sensory axons in the mouse, how loss of syndecan-1 impacts subbasal sensory nerve (SBN) innervation and reinnervation in the syndecan-1 null mouse cornea is not known.

Methods : The axon density of SBNs was quantified in unwounded as well as 1.5 mm trephine-only and debridement wounded corneas in wt and sdc1 null mice from 1-28 days after injury. For each wound type and time point a minimum of 5 corneas were assessed. SBN density was quantified in whole mount corneas stained to localize β3 tubulin. Confocal images were acquired and axon density quantified using the Sholl analysis. Significance was assessed by ANOVA.

Results : SBN axon density in the center and periphery of unwounded sdc1 null mice is reduced to 80% and 58% that of the control levels. The SBNs in trephine-only (crush) wounded sdc1 null corneas reinnervated slower over time than those in wt mice; in addition, after small wounds, SBNs reinnervated significantly slower in sdc1 null mice compared to wt mice after both wound types.

Conclusions : In unwounded sdc1 null mice, SBN density is reduced compared to wt mice. However, the vortex is retained. The SBNs of sdc1 null mice reinnervate slower after trephine only and debridement wounds. Previous studies have shown that reepithelialization of corneal debridement wounds of sdc1 null mice is slower and that they develop fewer recurrent erosions. These results show that sdc1 homologs (sdc2, sdc3, and sdc4) in the mouse likely compensate for the loss of sdc1 in the development and localization of SBNs in the mouse cornea.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.

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