| First Author | Sumioka T | Year | 2011 |
| Journal | Invest Ophthalmol Vis Sci | Volume | 52 |
| Issue | 5 | Pages | 2462-7 |
| PubMed ID | 21087965 | Mgi Jnum | J:171548 |
| Mgi Id | MGI:4950343 | Doi | 10.1167/iovs.10-5750 |
| Citation | Sumioka T, et al. (2011) Impaired angiogenic response in the cornea of mice lacking tenascin C. Invest Ophthalmol Vis Sci 52(5):2462-7 |
| abstractText | 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)beta1 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 TGFbeta1. 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 TGFbeta1 by exogenous TGFbeta1 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 TGFbeta1 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. |
