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. Author manuscript; available in PMC: 2021 Aug 1.
Published in final edited form as: Matrix Biol. 2020 Mar 12;90:79–108. doi: 10.1016/j.matbio.2020.02.004

Fig. 9. (A & B): Treatment of FNcKO LCs with exogenous active TGFβ1 restores the fibrotic response.

Fig. 9.

Fig. 9.

(A) Active TGFβ1 treated FNcKO capsular bags exhibit robust pSMAD2/3 levels (a measure of active TGFβ signaling) (***P ≤ 0.001), as well as robust expression of the fibrotic markers αSMA (**P = 0.001) and collagen I (**P ≤ 0.034) along with the profibrotic factor gremlin- (**P = 0.004) at 5 days PCS. In contrast, tenascin C deposition is not increased in FNcKO capsular bags after TGFβ1 treatment (P = 0.979) and the robust pSMAD1/5/8 levels indicative of active BMP signaling are also not affected at 5 days PCS (P = 0.286). (B) Treatment of FNcKO capsular bags with exogenous active TGFβ1 induces the upregulation of α5-integrin(***P ≤ 0.001), β1-integrin(**P 0.001), and αV-integrin expression (*P = 0.018), as well as pFAK levels (*P = 0.025), in FNcKO LCs at 5 days PCS. Collagen I, tenascin C, gremlin-1, pSMAD2/3 (downstream of TGFβ signaling), pSMAD1/5/8 (downstream of BMP signaling), α5-integrin, β1-integrin, αV-integrin, and pFAK (red) merged with αSMA (green) and DNA detected either by Draq5 or DAPI (blue). Scale bars: 35 μm; C, lens capsule; LC, remnant lens epithelial cells. All experiments had N = 3. Values are expressed as mean ± SEM. Asterisks (*) indicate statistically significant difference in MFI between WT and/or FNcKO and/or FNcKO (TGFβ1) at 5 days PCS..