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. 2015 Jan 22;290(10):6086–6105. doi: 10.1074/jbc.M114.601484

FIGURE 2.

FIGURE 2.

PI3K-C2α is required for TGFβ-induced Smad2/3 phosphorylation in EC but not smooth muscle cells or epithelial cells. A, TGFβ1-induced time-dependent phosphorylation of Smad2/3 and Smad1/5/8 in HMVECs. Serum-starved cells were stimulated with TGFβ1 (5 ng/ml) for the indicated time periods. The cell lysates were subjected to immunoblot analysis for p-Smad1/5/8 and p-Smad2/3. B, effects of Cre-mediated deletion of C2α on TGFβ1-induced Smad3 phosphorylation in MLECs. The cells were infected with adenoviruses encoding LacZ (Ad-LacZ) or Cre recombinase (Ad-Cre), stimulated as in A, and analyzed for p-Smad3. C, effects of Cre-mediated deletion of C2α on TGFβ1-induced Smad3 phosphorylation in MASM cells. The cells were treated and analyzed as in A. D, effects of knockdown of PI3K isoforms on TGFβ1-induced phosphorylation of Smad2/3. Caco2 were treated and analyzed as in A. In A–D, upper panels indicate representative blots, and lower panels indicate quantified data (n = 3–5). The data are expressed as multiples relative to the values in TGFβ1-nonstimulated sc-siRNA transfected cells or Ad-Cre-transfected cells.