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S. Tanaka, S. Saika, S. Kon, T. Uede, W. Kao, S. R. Rittling, D. T. Denhardt, Y. Ohnishi; Loss of Osteopontin Perturbs the Epithelial-Mesenchymal Transition in an Injured Mouse Lens Epithelium. Invest. Ophthalmol. Vis. Sci. 2007;48(13):4226.
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To investigate the role of osteopontin (OPN) in the wound healing process of the lens epithelium. We previously reported that OPN is up-regulated in the injured mouse lens prior to the epithelial-mesenchymal transition (EMT).
The role of endogenous OPN in the injury-induced EMT of the lens epithelium was examined by using a lens injury model in OPN-null (KO, n = 40) and wild-type (WT, n = 40) mice. The crystalline lens was punctured and the animals were killed at day 1, 2, 5 and 10 post-injury. Immunohistochemistry was employed to detect a-smooth muscle action (aSMA), collagen type I, transforming growth factor b1 (TGFb1), TGFb2 and phospho-Smad2/3. Cell proliferation was assayed by examining uptake of bromodeoxyuridine (BrdU).
Injury-induced EMT of mouse lens epithelium, as evaluated by histology, expression pattern of aSMA and collagen I, was altered in the absence of OPN with reduced phospho-Smad2/3 signaling; up-regulation of TGFb1 and TGFb2 was also inhibited. Cell proliferation was more active in KO mice as compared with WT mice at day 1 and 2, but not at day 5 and 10.
OPN is required for activation of Smad2/3 signal in an injured lens epithelium and lens cell EMT.
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