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. Author manuscript; available in PMC: 2021 Jul 1.
Published in final edited form as: Biochim Biophys Acta Mol Cell Res. 2020 Mar 14;1867(7):118703. doi: 10.1016/j.bbamcr.2020.118703

Figure 1. Constitutive expression of Smad2 and Smad3 in mouse tissues and in cultured cardiac fibroblasts.

Figure 1.

All mouse tissues had significant constitutive expression of Smad2 (A). The thymus (Th), pancreas (P), skin (Sk), spleen (Sp) and lung (Lu) had the highest levels of Smad2 expression (A, C). Constitutive expression of p-Smad2 was low in all organs studied (A). The skin (Sk), lung (Lu) and heart (H) had identifiable bands of p–Smad2 (A). Smad3 was also ubiquitously expressed in mouse tissues (B, D). The liver (Li), kidney (Ki) and heart (H) had the highest levels of Smad3 expression (B, D). Constitutive p-Smad3 expression was low in all organs studied. Relative expression of Smad2 (C) and Smad3 (D) was normalized to the total amount of protein, due to marked differences in baseline expression of the housekeeping protein GAPDH between tissues. Cultured cardiac fibroblasts (WT F) had high levels of baseline Smad2 and Smad3 expression, but low levels of Smad2 and Smad3 phosphorylation (A–B). TGF-β1 stimulation (TGF) triggered Smad2 and Smad3 phosphorylation in cardiac fibroblasts. Specificity of the antibodies was confirmed using Smad3 KO cells (S3KO F) (A–B). n=4.