June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Impairment of cornea epithelium wound healing in a TRPA1-deficient mouse
Author Affiliations & Notes
  • Yuka Okada
    Ophthalmology, Wakayama Medical University, Wakayama, Japan
  • Kumi Shirai
    Ophthalmology, Wakayama Medical University, Wakayama, Japan
  • Peter S Reinach
    Ophthalmology and Optometry, Wenzhou Medical University, Wenzhong, China
  • Masayasu Miyajima
    Laboratory Animal Center, Wakayama Medical University, Wakayama, Japan
  • Shizuya Saika
    Ophthalmology, Wakayama Medical University, Wakayama, Japan
  • Footnotes
    Commercial Relationships Yuka Okada, None; Kumi Shirai, None; Peter Reinach, None; Masayasu Miyajima, None; Shizuya Saika, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 703. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      Yuka Okada, Kumi Shirai, Peter S Reinach, Masayasu Miyajima, Shizuya Saika; Impairment of cornea epithelium wound healing in a TRPA1-deficient mouse. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):703.

      Download citation file:


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

      ×
  • Supplements
Abstract

Purpose: To examine if gene ablation of transient receptor potential ankyrin 1 (TRPA1), a cation channel receptor, affects healing of an experimental epithelial defect in a mouse cornea. TRPA1 is co-expressed with TRPV1 in corneal sensory nerve fibers and basal epithelial cells. We previously reported that gene knockout of TRPV1, another TRP family member, retarded epithelial healing in mice.

Methods: Healing of debridement of central corneal epithelium was examined in C57BL/6 (wild type, WT, n = 16) and TRPV1-null (KO, n = 16) mice. A round epithelial debridement (2.0 mm in diameter) was produced in the central cornea of the right eye in KO and WT mice. At healing intervals up to 36 hrs the remaining defect of the epithelium was determined by using green fluorescein staining. In another series of experiment the proliferation activity of the healing epithelium was determined by uisng BrdU-labeling in WT and KO mice. Real-time RT-PCR was performed in samples of the healing corneas to analyze the expression pattern of epithelial migration-related components, i. e., interleukin 6 (IL-6), substance P and transforming growth factor b1 (TGFb1).

Results: At 18 to 24 hrs post-debridement the defect remaining was larger in KO mice as compared with WT mice. BrdU-labeled cells were less frequently observed in KO healing epithelium as compared with WT cornea at 24 and 36 hrs post-wounding.Loss of TRPA1 suppressed expression of TGFb1 and substance P in response to epithelial debridement, but not of IL-6.

Conclusions: TRPA1 receptor-signal is required for healing of an epithelial debridement in association with suppression of cell proliferation and of up-regulation of gene expression of TGfb1 and substance P in mice.

×
×

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.

×