Figure 1: FAK is activated and directly associated with hypoxia-induced CF activation and phenotypic conversion in a dose-dependent and time-dependent manner. | Scientific Reports

Figure 1: FAK is activated and directly associated with hypoxia-induced CF activation and phenotypic conversion in a dose-dependent and time-dependent manner.

From: Targeted inhibition of Focal Adhesion Kinase Attenuates Cardiac Fibrosis and Preserves Heart Function in Adverse Cardiac Remodeling

Figure 1

(a) α-SMA and vimentin was gradually increased with time, indicative of transformation to a myofibroblast phenotype. serum-starved and hypoxia-induced CFs had a significantly higher baseline level of p-FAK in a time-dependent manner. (b) Using PF-573228 at a concentration range of 0.01–10 μM for 24 hours decreased phosphorylated FAK expression in a time-dependent manner, and there was a 70% inhibition rate at the range of 5–10 μM. (c–e) Densitometric analysis of blots for determining α-SMA and Vimentin normalized to GAPDH, pY397 of FAK levels were normalized to total FAK levels. (f) Densitometry of inhibition level of p-FAK activation from Panel b. Multiple exposures of vimentin and GAPDH are presented in Supplementary Figure S6; full-length blots are presented in Supplementary Figure S1 (1a,1b). Data are presented as means ± SEM. ***P < 0.001.

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