Atherogenic ω-6 Lipids Modulate PPAR- EGR-1 Crosstalk in Vascular Cells
Figure 1
ω-6 lipids modulate PPAR protein levels and PPRE transactivity in a time-dependent manner. Western blotting of RASMC lysates treated with 10–50 μM of LA and OxLA for 0–12 hrs using PPARα and PPARγ antibody shows induction of PPARα at acute phase and PPARγ at subacute phase. Control (CTRL) was defined as the cells treated with vehicle only. The results were expressed as mean ± SEM (Standard Error of Mean) defined by the ratio of protein levels in treated samples compared to CTRL. All data were normalized to β-actin (house-keeping protein) (a) PPARα protein levels after 1 hr, 4 hr, 12 hrs treatment. (b) PPARγ protein levels after 1 hr, 4 hr, 12 hrs treatment. The figure is a representation of three independent blots. One way ANOVA was used for the comparison between two treatments. Significance was confirmed using post hoc analysis using Fisher LSD test. *. (c) PPAR transactivity was measured in PPRE-luciferase transfected RASMCs which were pretreated with 10 μM MK886 (PPARα antagonist) or 1 μM GW9662 (PPARγ antagonist) followed by exposure to 10–50 μM LA or OxLA for 4 hrs. The assay were run in duplicates and repeated three independent times. The results were expressed as mean relative luciferase activity ± SEM (Standard Error of Mean). One way ANOVA was used for the comparison between two treatments. Significance was confirmed using post hoc analysis using Fisher LSD test. *compared to CTRL, ; #compared to 10 μM concentration, .
