Fig. 2

HDAC4 promotes airway inflammation and remodeling by increasing KLF5 transcriptional activity through deacetylation. a The expression of HDAC4 in BEAS-2B and HBE cells with different treatment as determined by RT-qPCR. b The acetylation level of HDAC4 and KLF5 as determined by Western blot assay. c The binding between HDAC4 and KLF5 as examined by IP assay. d The transcription activity of KLF5 as examined by dual luciferase reporter gene assay. e The expression of TGF-β and inflammatory factors IL-4, IL-5, and IL-13 in the supernatant of BEAS-2B and HBE cells with different treatment as examined by ELISA. f The proliferation of BSMCs with different treatment as examined by CCK-8 assay. g The proliferation of BSMCs with different treatments as examined by Transwell. *p < 0.05 vs. control or control-CM. #p < 0.05 vs. OVA + sh-NC. &p < 0.05 vs. OVA + sh-HDAC4 + vector. These data are measurement data, expressed as mean ± standard deviation. Data among multiple groups were compared using one-way ANOVA, combined with Tukey’s post-hoc tests