Figure 11

Spry can prevent TGFβ-induced EMT leading to anterior subcapsular cataract formation. Representative sections of postnatal-d-10 WT mouse lenses (A, A’, B, B’) or transgenic mouse lenses overexpressing TGFβl (C, C’, D, D’; TGFβ) or both TGFβl and Spry1 (E, E’, F, F’; TGFβ/Spry1), immunolabelled for either α-sma (A’, C’, E’) or E-cadherin (B’, D’, F’), with cell nuclei counterstained with Hoechst dye (A–F). Compared to WT lens epithelia (le) that are nonreactive for α-sma (A’), lens cells in transgenic mice stimulated by elevated levels of TGFβ express α-sma (C’) as they undergo an EMT to form anterior subcapsular plaques (C). Consistent with this observation, the normal membrane distribution of E-cadherin in lens epithelial cells of WT mice (B’) is reduced and lost in transgenic mice overexpressing TGFβ (D’) as the cells multilayer and undergo an EMT (D). In lens epithelial cells (le) of transgenic mice overexpressing TGFβ and Spry, there is no immunolabeling for α-sma (E’) in this monolayer (E, F) and immunolabeling for E-cadherin (F’) is retained in these cells, similar to that seen in the epithelia of WT mice. Scale bar, 20 µm.