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Updated: Mar 31, 2026
A Mouse Model for Laser-induced Choroidal Neovascularization
Published on: December 27, 2015
Suppression of In Vivo Neovascularization by the Loss of TRPV1 in Mouse Cornea
Katsuo Tomoyose1, Yuka Okada1, Takayoshi Sumioka1
1Department of Ophthalmology, Wakayama Medical University, 811-1 Kimiidera, Wakayama 641-0012, Japan.
Abstract:
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.
Insights
Loss of the TRPV1 receptor inhibits corneal neovascularization by reducing angiogenic growth factors. This finding is crucial for understanding blood vessel development in the cornea.
Area of Science:
- Ophthalmology
- Molecular Biology
- Immunology
Background:
- Transient receptor potential vanilloid 1 (TRPV1) is a receptor involved in various physiological processes.
- Neovascularization, or the formation of new blood vessels, is a critical process in corneal wound healing but can lead to vision impairment.
- The role of TRPV1 in corneal neovascularization remains incompletely understood.
Purpose of the Study:
- To investigate the impact of TRPV1 deficiency on the development of corneal neovascularization in a mouse model.
- To elucidate the underlying molecular mechanisms by which TRPV1 influences angiogenic processes in the cornea.
Main Methods:
- Utilized a mouse model with TRPV1 gene ablation (TRPV1 knockout).
- Induced corneal neovascularization via cauterization.
- Assessed neovascularization using immunohistochemistry for active TGFβ1 and VEGF.
- Quantified mRNA expression of VEGF and TGFβ1 in corneal tissues.
- Evaluated immune cell infiltration (neutrophils and macrophages).
- Performed in vitro experiments using human umbilical vein endothelial cells (HUVECs).
Main Results:
- TRPV1 deficiency significantly inhibited neovascularization in the corneal stroma following cauterization.
- While VEGF-dependent neovascularization was unaffected in cell culture by TRPV1 blockade, in vivo studies showed reduced immunoreactivity for active TGFβ1 and VEGF in TRPV1 knockout mice.
- mRNA expression of VEGF and TGFβ1 was suppressed in the corneas of mice lacking TRPV1.
- TRPV1 gene ablation did not alter neutrophil or macrophage invasion into the cauterized cornea.
- In vitro, blocking TRPV1 did not affect angiogenic effects by HUVECs.
Conclusions:
- TRPV1 signaling is involved in the expression of angiogenic growth factors in the context of corneal injury.
- TRPV1 is essential for neovascularization in the corneal stroma in vivo, likely through its regulation of angiogenic factor expression.
- Targeting TRPV1 may offer a therapeutic strategy for controlling pathological corneal neovascularization.
