Research Paper Volume 12, Issue 9 pp 8339—8351

Transcription factor YY1 inhibits the expression of THY1 to promote interstitial pulmonary fibrosis by activating the HSF1/miR-214 axis

Figure 1. HSF1 knockdown may suppress the proliferation and fibrogenic transformation of HEPFs. (A) The YY1 expression in HEPFs transfected with three si-YY1 sequences determined at mRNA and protein levels by RT-qPCR and western blot analysis, respectively. *, p < 0.05 vs. cells transfected with si-NC. (B) The expression of YY1 and HSF1 in the HEPFs co-transfected with si-YY1/si-NC and oe-HSF1/oe-NC measured at mRNA and protein levels by RT-qPCR and western blot analysis, respectively. *, p < 0.05 vs. cells treated with si-NC and oe-NC. (C) The viability of HEPFs co-transfected with si-YY1/si-NC and oe-HSF1/oe-NC assessed by CCK8 experiment. *, p < 0.05 vs. cells after treatment of si-NC and oe-NC, #, p < 0.05 vs. cells transfected with si-YY1 and oe-NC. (D) The expression of cell proliferation marker Ki67 and fibrosis biomarkers CoI, CoIII, α-SMA and vimentin in the HEPFs co-transfected with si-YY1/si-NC and oe-HSF1/oe-NC measured at mRNA and protein levels by RT-qPCR and western blot analysis, respectively. *, p < 0.05 vs. cells co-transfected with si-NC and oe-NC, #, p < 0.05 vs. cells co-transfected with si-YY1 and oe-NC. Statistical data were measurement data, and presented as mean ± standard deviation. Unpaired t-test was used for comparison between the two groups, and one-way ANOVA with Tukey's post hoc test was employed for comparisons among multiple groups. The experiment was independently repeated three times.