Fig. 4

Co-culture with UC/PL-MSC-CM inhibits TGF-β1-induced fibrogenic activation of HIMFs. HIMFs were treated with TGF-β1 (5 ng/mL) and co-cultured with or without UC/PL-MSC-CM. A RT-qPCR analysis of the relative mRNA expression of collagen1A1 (COL1A1), fibronectin (FN1), and α-smooth muscle actin (ACTA2). The data were normalized to GAPDH expression and expressed as relative values compared to the control (n = 3). B Representative Western blots show the protein expression of procollagen1A1 (Procol1A1), fibronectin (FN), α-smooth muscle actin (α-SMA), and phosphorylated Smad2 (p-Smad2) with GAPDH as a loading control. C Quantitation of Procol1A1, FN, α-SMA, and p-Smad2 from Western blot analyses (n = 4). Data are expressed as means ± SEM. ^##P < .01 and ^###P < .001 versus the control; ^*P < .05, ^**P < .01, and ^***P < .001 versus the TGF-β1 treatment only (ANOVA w/ Tukey); ^†P < .05 compared between PL-MSC-CM and UC-MSC-CM (Mann–Whitney U test). NS, not significant. Full-length blots are presented in Additional file 1: Fig. S3