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S. Tanaka, K.-I. Miyazaki, S. Saika; Loss of Tenascin-c Perturbs the Epithelial-Mesenchymal Transition in an Injured Mouse Lens Epithelium. Invest. Ophthalmol. Vis. Sci. 2008;49(13):2774. doi: https://doi.org/.
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© ARVO (1962-2015); The Authors (2016-present)
To investigated the role of tenascin-C in epithelial-mesenchymal transition (EMT) of the lens epithelium during wound healing in mice.
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.
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.
Injury-induced EMT of mouse lens epithelium and expression of collagen I and TGFβ were attenuated by lacking tenascin C
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