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. 2022 May 7;10(5):1089. doi: 10.3390/biomedicines10051089

Figure 6.

Figure 6

FIR treatment regulates TGF-β1-induced EndoMT via Smad- and Slug-dependent pathways. (A,B) Human EPCs were exposed to 2 or 10 μg/mL recombinant human TGF-β1 for 5 days with high intensity or without FIR treatment. The α-SMA, VE-cadherin, vWF, and vimentin mRNA expression were evaluated using reverse transcription and qPCR analysis. The expression of related mRNA expression is normalized to the expression of GAPDH mRNA, is presented as a bar graph. All data are expressed as the mean ± SD of five independent experiments and as the percentage of the control. * p < 0.05 was taken into consideration statistically considerable. (C,D) Human EPCs were exposed to 10 μg/mL TGF-β1 for 5 days with low intensity, high intensity or without FIR treatment. The total protein expression of the vWF, VE-cadherin, α-SMA, vimentin, and phosphorylated Smad2 were identified by Western blot analysis. β-actin and total-Smad2 were used as loading controls. (E) Human EPCs were treated with 10 μg/mL TGF-β1 in the presence or absence of FIR treatment for 5 days. Total nuclear lysates were purified, and the levels of Snail and Slug were analyzed using Western blotting; lamin A/C was used as a loading control.