April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
Systemic administration of TRPV4 antagonist suppresses corneal inflammation and scarring induced by alkali burning in mice.
Author Affiliations & Notes
  • Yuka Okada
    Ophthalmology, Wakayama Medical University, Wakayama, Japan
  • Kumi Shiai
    Ophthalmology, Wakayama Medical University, Wakayama, Japan
  • Masayasu Miyajima
    The Laboratory Animal Center, Wakayama Medical University, Wakayama, Japan
  • Peter S Reinach
    Pharmacology, Faculty of Medicine of Ribeirao Preto University of Sao Paulo, Ribeirao Preto, Brazil
  • Shizuya Saika
    Ophthalmology, Wakayama Medical University, Wakayama, Japan
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 4683. doi:
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      Yuka Okada, Kumi Shiai, Masayasu Miyajima, Peter S Reinach, Shizuya Saika; Systemic administration of TRPV4 antagonist suppresses corneal inflammation and scarring induced by alkali burning in mice.. Invest. Ophthalmol. Vis. Sci. 2014;55(13):4683.

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

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Abstract

Purpose: We previously reported that in mice transient receptor potential vanilloid 4 (TRPV4) gene ablation improved the corneal wound healing response to alkali burning (ARVO, 2011). We here tried to reproduce its favorable effects by using a TRPV4 antagonist.

Methods: Three microliters of 1 N NaOH were applied to the right eye of WT (n = 24) mice to produce an ocular surface alkali burn under general anesthesia. The mice received intraperitoneal injection of either a TRPV4 receptor antagonist, HC-067047 (10 mg/kg, daily), or its vehicle. The eyes were processed for histology/immunohistochemistry.

Results: Stroma of the TRPV4 antagonist-treated WT mice healing corneas were less opaque as compared with those of untreated WT mice at 5 to 20 days post-alkali burn. Hematoxylin-eosin histological staining indicated more marked inflammation in the thickened stroma of untreated WT mice. Immunohistochemical examination showed less population of cells of immunoreaction for α-smooth muscle actin expression, F4/80, myeloperoxidase and active TGFβ1 in the TRPV4 antagonist-treated WT mice after alkali burn.

Conclusions: Systemic TRPV4 antagonist administration reproduced the KO healing phenotype; suppression of inflammation and scarring in the alkali-burned corneal stroma. This favorable outcome could mean that TRPV4 is a potential drug target for reducing the adverse effects of TRPV4 activation by injury.

Keywords: 765 wound healing • 557 inflammation • 484 cornea: stroma and keratocytes  
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