September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Effects of loss of TRPV4 function on corneal epithelial wound healing in mice.
Author Affiliations & Notes
  • Yuka Okada
    Ophthalmology, Wakayama Medical University, Wakayama, Wakayama, Japan
  • Peter S Reinach
    Wenzhou Medical University, Wenzhou, China
  • Masayasu Miyajima
    Laboratory Animal Center, Wakayama Medical University, Wakayama, Japan
  • Shizuya Saika
    Ophthalmology, Wakayama Medical University, Wakayama, Wakayama, Japan
  • Footnotes
    Commercial Relationships   Yuka Okada, None; Peter Reinach, None; Masayasu Miyajima, None; Shizuya Saika, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science September 2016, Vol.57, 1253. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to Subscribers Only
      Sign In or Create an Account ×
    • Get Citation

      Yuka Okada, Peter S Reinach, Masayasu Miyajima, Shizuya Saika; Effects of loss of TRPV4 function on corneal epithelial wound healing in mice.. Invest. Ophthalmol. Vis. Sci. 2016;57(12):1253.

      Download citation file:


      © 2017 Association for Research in Vision and Ophthalmology.

      ×
  • Supplements
Abstract

Purpose : To determine if transient receptor potential vanilloid 4 (TRPV4), TRPV1-related component, contributes to epithelial wound healing in a mouse cornea. Growth factor expression pattern was also evaluated. TRP family consists of groups of TRPV, ankyrin 1 (TRPA1) or melastatin (TRPM). We previously reported the involvement of TRPV1 and TRPA1 in corneal epithelial wound healing in mice (IOVS 2014, ARVO 2015).

Methods : Imunohistochemistry was carried out to examine the expression opattern of TRPV4 in mouse cornea. Time dependent closure of a 2.0 mm diameter central corneal epithelial debridement was monitored in the right eyes of C57BL/6 (wild type, WT, n =61) and TRPV4-null (KO, n =61) mice for up to 36 h using fluorescein green staining. BrdU-labeling in WT and KO mice evaluated proliferative activity during healing. RT-PCR analyzed interleukin 6 (IL-6), substance P (SP) calcitonin gene-related peptide (CGRP), nerve growth factor (NGF) and transforming growth factor b1 (TGFb1) gene expression levels.

Results : TRPV4 was detected in the basal cells of the corneal epithelium. The open wound area in the TRPV4 KO mice at 18 and 24 hr was 1.6-fold and 7.34-fold bigger than in the WT counterpart, respectively. BrdU-labeled cells were fewer in the KO healing epithelium than in the WT counterpart at 24 and 36 hr (p<0.05). Increases in CGRP, NGF and TGFb1 gene expression were smaller than those in the WT counterpart (p<0.05) whereas increases in IL-6 and SP were unaffected by the loss of TRPV4 function.

Conclusions : TRPV4 mediated signaling contributes to increases in CGRP, NGF and TGFb1 gene expression and repair of a corneal epithelial debridement in mice.

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

×
×

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.

×