Figure 7
From: Impaired cornea wound healing in a tenascin C-deficient mouse model
Expression of fibrogenic components in the ocular fibroblasts derived from post-natal day 1 (P1) wild-type (WT) and tenascin C-null (knockout (KO)) mice. Exogenous transforming growth factor β1 (TGFβ1) at 1.0 ng/ml upregulates mRNA expression of collagen Iα1 (a) and TGFβ1 (b), but not TGFβ2 (c) in WT ocular fibroblasts, and also increases TGFβ1 mRNA expression in KO cells (b). The loss of tenascin C counteracts the upregulation of collagen Iα1 and TGFβ1 by adding TGFβ1. Expression of α-smooth muscle actin (αSMA) is the hallmark of myofibroblast generation and tissue fibrosis. Adding exogenous TGFβ1 enhances expression of αSMA mRNA, which is counteracted by lacking tenascin C in cultured ocular fibroblasts (d). Western blotting further shows that exogenous TGFβ1 increase protein expression of αSMA and this promotion is counteracted by the loss of tenascin C. **P<0.01.
