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. 2018 Aug 23;3(16):e120398. doi: 10.1172/jci.insight.120398

Figure 4. TGF-β is activated in RA-deficient ASM.

Figure 4

(A and B) Immunostaining of phospho-SMAD2 (p-SMAD2) showing signals within the ASM layer of BMS (B) but not CTR (A) airway, indicating activation of TGF-β signaling in RA-deficient mouse ASM (n = 3 per group). Scale bar: 20 μm. (C) p-SMAD2 to total SMAD2 (tSMAD2) ratio is increased in BMS- and DEAB-treated hASM compared with hASM cultured in CTR medium, indicating higher level of TGF-β activity in the RA-deficient hASM (n = 3). (D) Expression of COL1A2, a transcriptional target of TGF-β signaling, is increased in VAD mASM (compared with VAS mASM) and BMS mASM (compared with CTR mASM) (n = 3 per group). (E) COL1A2 production is increased with BMS- and DEAB-treated hASM compared with CTR hASM (n = 3). Data represent the mean ± SEM. Student’s t test was used to calculate P values in D (*P < 0.05). Two-way ANOVA was used for statistical analysis in C and E where P values were adjusted by Bonferroni’s correction (means with different letters are significantly different with P < 0.05).