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Journal of Ophthalmology
Volume 2015, Article ID 706404, 9 pages
Research Article

Suppression of In Vivo Neovascularization by the Loss of TRPV1 in Mouse Cornea

1Department of Ophthalmology, Wakayama Medical University, 811-1 Kimiidera, Wakayama 641-0012, Japan
2Laboratory Animal Center, Wakayama Medical University, 811-1 Kimiidera, Wakayama 641-0012, Japan
3Laboratory of Cell Regulation and Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
4Wenzhou Medical University School of Ophthalmology and Optometry, Wenzhou, China

Received 10 December 2014; Revised 6 March 2015; Accepted 16 March 2015

Academic Editor: Caio V. Regatieri

Copyright © 2015 Katsuo Tomoyose et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


To investigate the effects of loss of transient receptor potential vanilloid receptor 1 (TRPV1) on the development of neovascularization in corneal stroma in mice. Blocking TRPV1 receptor did not affect VEGF-dependent neovascularization in cell culture. Lacking TRPV1 inhibited neovascularization in corneal stroma following cauterization. Immunohistochemistry showed that immunoreactivity for active form of TGFβ1 and VEGF was detected in subepithelial stroma at the site of cauterization in both genotypes of mice, but the immunoreactivity seemed less marked in mice lacking TRPV1. mRNA expression of VEGF and TGFβ1 in a mouse cornea was suppressed by the loss of TRPV1. TRPV1 gene ablation did not affect invasion of neutrophils and macrophage in a cauterized mouse cornea. Blocking TRPV1 signal does not affect angiogenic effects by HUVECs in vitro. TRPV1 signal is, however, involved in expression of angiogenic growth factors in a cauterized mouse cornea and is required for neovascularization in the corneal stroma in vivo.