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Updated: Jun 6, 2026
The Corneal Micropocket Assay: A Model of Angiogenesis in the Mouse Eye
Published on: August 16, 2014
Impaired angiogenic response in the cornea of mice lacking tenascin C
Takayoshi Sumioka1, Norihito Fujita, Ai Kitano
1Department of Ophthalmology, Wakayama Medical University, 811-1 Kimiidera, Wakayama, 641-0012, Japan. sumioka@wakayama-med.ac.jp
Purpose:
This study investigated the effects of loss of tenascin C (TNC) in the development of neovascularization in a corneal stroma in mice. Cell culture study was also conducted to clarify the roles of TNC in the expression of vascular endothelial growth factor (VEGF) and transforming growth factor (TGF)β1 in fibroblasts and macrophages.
Methods:
Ocular fibroblasts and macrophages from wild-type (WT) and TNC-null (KO) mice were used to study the role of TNC in the expression of VEGF and TGFβ1. The effects of the absence of TNC on angiogenic gene expression, inflammatory cell invasion, and cornea neovascularization in the corneal stroma were then evaluated after cauterization of the center of the cornea in mice. Histologic, immunohistochemical, and mRNA expression analyses were performed.
Results:
Absence of TNC suppressed expression of VEGF and counteracted upregulation of TGFβ1 by exogenous TGFβ1 in ocular fibroblast culture. Such effects of the absence of TNC were not observed in cultured macrophages. Absence of TNC attenuated expression of both VEGF and TGFβ1 mRNA as well as neovascularization into the stroma after cauterization at the center of the cornea in mice. Absence of TNC suppressed macrophages, but not neutrophils, invading the cauterized cornea.
Conclusions:
TNC is involved in angiogenic gene expression in ocular fibroblasts in vitro and in vivo and is required for macrophage invasion and neovascularization of injured corneal stroma.
Insights
Loss of tenascin C (TNC) suppresses vascular endothelial growth factor (VEGF) and transforming growth factor-beta1 (TGFβ1) expression in ocular fibroblasts, inhibiting corneal neovascularization and macrophage invasion.
Area of Science:
- Ophthalmology
- Cell Biology
- Immunology
Background:
- Neovascularization is a complex process involving the formation of new blood vessels.
- Tenascin C (TNC) is an extracellular matrix protein implicated in various biological processes, including wound healing and inflammation.
- Understanding the role of TNC in corneal neovascularization is crucial for developing therapeutic strategies.
Purpose of the Study:
- To investigate the role of TNC in corneal neovascularization.
- To elucidate the effects of TNC on the expression of vascular endothelial growth factor (VEGF) and transforming growth factor-beta1 (TGFβ1) in ocular fibroblasts and macrophages.
Main Methods:
- Ocular fibroblasts and macrophages from wild-type and TNC-null mice were cultured.
- TNC's effect on VEGF and TGFβ1 expression was assessed in vitro.
- Corneal neovascularization was induced by cauterization in mice, and histological, immunohistochemical, and mRNA analyses were performed.
Main Results:
- Absence of TNC suppressed VEGF expression and counteracted TGFβ1 upregulation in ocular fibroblasts.
- TNC deficiency attenuated VEGF and TGFβ1 mRNA expression and reduced neovascularization in the cornea.
- TNC absence inhibited macrophage, but not neutrophil, invasion into the injured cornea.
Conclusions:
- TNC plays a significant role in regulating angiogenic gene expression in ocular fibroblasts.
- TNC is essential for macrophage recruitment and neovascularization in the injured corneal stroma.
- Targeting TNC may offer a therapeutic approach for managing corneal neovascularization.
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