Fig. 1
From: Integrin activation by the lipid molecule 25-hydroxycholesterol induces a proinflammatory response
FAK-NFκB pathway is required for 25HC-dependent proinflammatory response. a Structure of 25-hydroxycholesterol (25HC). b–g Cells were treated with 50 µM 25HC for 8 h. FAK and NFκB activation and proinflammatory response in treated cells were evaluated. b Western blot and densitometric analyses of FAK activation (phospho-FAK, Tyr925) status in 25HC-treated RAW 264.7 macrophages. c IL-6 secretion from wild-type (WT) and FAK knockout (KO) MEFs (mouse embryo fibroblasts) treated with 25HC. d TNF secretion from NR-9456 macrophages treated with 25HC in the absence or presence of FAK inhibitor (5 µM). e TNF secretion from BMDMs treated with 25HC in the absence or presence of NFκB inhibitor Bay 11-7082 (BAY-11) (10 µM). f TNF secretion from WT and NFκB p105 KO BMDMs treated with 25HC. g Western blot and densitometric analyses of phospho-IκB status in 25HC-treated WT and FAK KO MEFs. The ELISA values (mean ± standard deviation) are representative from two or three independent experiments (n = 4). *p ≤ 0.05 using a Student’s t-test. The densitometric quantification values for phospho-FAK (p-FAK) and phospho-IκB (p-IκB) immunoblots represent the ratio of phospho-FAK:actin and phospho-IκB:actin and the fold-induction was calculated after normalizing with the control untreated (UT) or control 0 h group. The densitometric values represent the mean ± standard deviation from three independent studies. *p ≤ 0.05 using a Student’s t-test
