Fig 1: BET proteins regulate expression of key drivers of fibrosis in HRMCs. HRMCs were treated with TGF-ß1 ± BETi or TGFBRi for 24 h, followed by gene expression analysis by real-time PCR (left column (A,C,E,G); n = 4 or 5). For secreted proteins (right column (B,D,F,H)), HRMCs were treated for 48 h. Cell culture media were clarified of debris by centrifugation, and the indicated proteins quantified by ELISA (n = 3). Data are presented as mean ± SD. Statistical analysis by one-way ANOVA followed by Dunnett’s Multiple Comparison Test. * p < 0.05, ** p < 0.01, *** p < 0.001, NS not significant. THBS1: thrombospondin 1 gene. FN1: fibronectin gene. POSTN: periostin gene. SPARC gene and SPARC protein: secreted protein acidic and rich in cysteine. TGF-ß1: Transforming growth factor ß1. Apabetalone: BD2-selective BET inhibitor. JQ1: pan-BET inhibitor. MZ1: PROTAC that directs BET proteins for degradation.