Abstract
Purpose: :
To investigated the role of tenascin-C in epithelial-mesenchymal transition (EMT) of the lens epithelium during wound healing in mice.
Methods: :
The crystalline lens in one eye was injured by needle puncture in tenascin-C-null (KO, n = 40) and wild-type (WT, n = 40) mice under both general and topical anesthesia. The animals were killed at day 1, 2, 5 and 10 post-injury. Immunohistochemistry was employed to detect tenescin-C, α-smooth muscle action (alpha-SMA), a marker of EMT, collagen type I, transforming growth factor β1 (TGFβ1), TGFβ2.
Results: :
WT lens epithelial cells up-regulate tenascin C and the underwent EMT post-puncture injury as evaluated by histology and immunohistochemistry for alpha-SMA or tenascin C. At up to day 2 both WT and KO lens epithelium exhibited an epithelilal shape and lacked alpha-SMA expression. At day 5 WT lens epithelial cells exhibited elongated fibroblastic morphology with marked expressed alpha-SMA, while KO cells were still of epithelium in histology and lacked alpha-SMA expression. At day 10 both WT and KO cells showed an elongated fibroblastic appearance with alpha-SMA expression, indicating an establishment of EMT.
Conclusions: :
Injury-induced EMT of mouse lens epithelium and expression of collagen I and TGFβ were attenuated by lacking tenascin C
Keywords: EMT (epithelial mesenchymal transition) • pathobiology • wound healing