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. 2022 Aug 16;11(16):2540. doi: 10.3390/cells11162540

Figure 8.

Figure 8

OGR1 does not inhibit Smad2 phosphorylation in 16-HBEs but does so in fibroblasts. Here, 16-HBE cells were transfected with either GFP or OGR1 plasmids and subsequently treated with TGF-β. Canonical TGF-β signaling was then assessed by western blot, examining changes in phosphorylated Smad2 relative to total Smad2. Although TGF-β significantly increased phosphorylated levels of Smad2 (A, **** p < 0.0001), overexpression of OGR1 was unable to mitigate TGF-β-induced Smad2 phosphorylation (A, **** p < 0.0001). Fibroblasts underwent identical transfection and treatment, and TGF-β significantly increased Smad2 phosphorylation (B, *** p = 0.0007). However, in the presence of OGR1 overexpression, TGF-β was unable to phosphorylate Smad2 (B, difference between Con and OGR1 + TGF-β, p = 0.0031 by Student’s t-test). Data represent mean expression ± SEM. Open circles represent control plasmid and closed circles represent control plasmid plus TGF-β. Open diamonds represent OGR1 plasmid and closed diamonds represent OGR1 plasmid plus TGF-β.