Figure 7. FAK inhibition blocks wire injury-induced upregulation of DNMT3A and 5-mC levels and maintains expression of SMC-specific contractile genes.

(A) Mice were treated with vehicle or FAK-I (VS-4718, 50 mg/kg) twice daily for 2 weeks following wire injury. Representative immunoblots of femoral artery lysates from (A) FAK-I treated or (B) FAK-WT and -KD mice 2 weeks following injury for pY397 FAK, FAK, DNMT3A, DNMT3B, DNMT1, MYH11, CALD1, ACTA2, CNN1, TAGLN and GAPDH as loading control (n=4). pY397 FAK blots were quantified relative to total FAK, and other blots to GAPDH. (C) Representative dot blots for 5-mC using gDNA isolated from femoral arteries with or without FAK-I treatment 2 weeks postinjury (n=3). The methylene blue (MB) staining of 150 ng total genomic DNA was used as loading control. (D) SMCs were treated with either vehicle or FAK-I for 24 h. Chromatin immunoprecipitation (ChIP) on Myh11, Tagln, and Acta2 promoters was performed with the indicated histone and SRF antibodies (n=3). Data are mean±SEM. P values were determined using t-test (D).