Skip to main content
. 2015 Jun;5(2):382–397. doi: 10.1086/681272

Figure 6.

Figure 6

10T1/2 cell differentiation to a smooth muscle phenotype is transforming growth factor (TGF)–β dependent. A, Immunostaining for α–smooth muscle actin (SMA), γ-SMA, SM22α, and smooth muscle myosin heavy chain (SMMHC; all positive reactions are green) in 10T1/2 cells, with or without TGF-β1 treatment, in the presence or absence of a TGF-β type I receptor (TGF-βRI) inhibitor (LY364947). Scale bar = 10 μm. B, α- and γ-SMA messenger RNA expression in 10T1/2 cells after stimulation with TGF-β1, with or without LY364947. Plasminogen activator inhibitor type 1 (PAI-1) was used as a positive control for canonical TGF-β signaling activation. Signals were normalized to GAPDH. C, Western immunoblotting for α- and γ-SMA expression in 10T1/2 cells after stimulation with TGF-β1, with or without a TGF-βRI inhibitor (SB431542). Phosphorylation of Smad2 (P-Smad2) was examined as a marker of canonical TGF-β signaling. GAPDH was used as a loading control.