Monounsaturated fatty acids protect against palmitate-induced lipoapoptosis in human umbilical vein endothelial cells

Figures

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  Fig 1. The saturated fatty acid palmitate decreases viability and induces apoptosis in HUVECs. Fold change from control in a) viability and b) apoptosis after treatment with palmitate (PA) at 0.25 or 0.5mM. Data are expressed as mean±SEM; n = 7–8 independent experiments; #p<0.05 vs all.

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  Fig 2. The monounsaturated fatty acid oleate prevents detrimental effects of palmitate. Fold change from control in a) viability and b) apoptosis after treatment with palmitate (PA) at 0.25 or 0.5mM, or co-treatment with the unsaturated fatty acid oleate (Ole). Data are expressed as mean±SEM; n = 4–5 independent experiments; *p<0.05 vs control.

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  Fig 3. The monounsaturated fatty acid palmitoleate prevents detrimental effects of palmitate. Fold change from control in a) viability and b) apoptosis after treatment with palmitate (PA) at 0.25 or 0.5mM, or co-treatment with the unsaturated fatty acid palmitoleate (PO). Data are expressed as mean±SEM; n = 4–6 independent experiments; *p<0.05 vs control.

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  Fig 4. The monounsaturated fatty acid oleate prevents palmitate-induced markers of cellular adhesion and ER stress. Fold change from control in a) ICAM-1, b) E-selectin and c) sXBP1 expression after treatment with palmitate (PA) at 0.25 or 0.5mM, or co-treatment with the unsaturated fatty acid oleate (Ole). Data are expressed as mean±SEM, n = 3 independent experiments, *p<0.05 vs control.

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  Fig 5. The small molecule IRE1 inhibitor 4μ8C or ER stress inhibitor TUDCA, do not prevent the detrimental effects of palmitate. Fold change from control in a) viability and b) apoptosis after treatment with palmitate (PA) at 0.5mM or co-treatment with the IRE1 inhibitor 4μ8C at 0.06mM. Fold change from control in a) viability and b) apoptosis after treatment with palmitate (PA) at 0.5mM or co-treatment with TUDCA at 1 and 5mM. Data are expressed as mean±SEM, n = 2–4 independent experiments, *p<0.05 vs control.

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  Fig 6. The AMPK activator AICAR prevents detrimental effects of palmitate. Cells were pretreated with AICAR (0.1 or 0.5mM) for 2hr then co-incubated with palmitate (PA). Fold change from control in a) viability and b) apoptosis after treatment with palmitate (PA), AICAR, or a combination of both. Data are expressed as mean±SEM; n = 2–6 independent experiments; *p<0.05 vs control, #p<0.05 vs both PA concentrations.

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  Fig 7. The AMPK activator AICAR attenuates palmitate-induced markers of cellular adhesion and ER stress. Cells were pretreated with AICAR (0.5mM) for 2hr then co-incubated with palmitate (PA). Fold change from control in a) ICAM-1, b) ATF4, c) ATF5, d) GADD34, e) GRP78 and f) CHOP expression after treatment with palmitate (PA) 0.25 and 0.5mM, or co-treatment with the AMPK activator AICAR (0.5mM). Data are expressed as mean±SEM, n = 3 independent experiments, *p<0.05 vs control.

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  Fig 8. The AMPK inhibitor CC exacerbates palmitate-induced decreases in viability. Cells were pretreated with compound C (CC; 20 or 40μM) and then co-incubated with palmitate (PA). Fold change from control in a) viability and b) apoptosis after treatment with palmitate (PA), compound C (CC), or a combination of both. Data are expressed as mean±SEM; n = 3–5 independent experiments; *p<0.05 vs control, #p<0.05 vs both PA concentrations.

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  Fig 9. The AMPK inhibitor CC prevents protective effects of AICAR against palmitate. Cells were pretreated with AICAR (0.1 or 0.5mM) alone or in combination with compound C (CC; 20 or 40μM) and then co-incubated with palmitate (PA). Fold change from control in a) viability and b) apoptosis after treatment with palmitate (PA), compound C (CC), and AICAR. Data are expressed as mean±SEM; n = 3–6 independent experiments; *p<0.05 vs control, #p<0.05 vs PA+AICAR at equimolar doses.

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  Fig 10. The AMPK inhibitor CC prevents protective effects of the monounsaturated fatty acids oleate and palmitoleate. Cells were pretreated with compound C (CC; 20 or 40μM) and then co-incubated with a combination of palmitate (PA) and oleate (Ole) or palmitoleate (PO). Fold change from control in a) viability with Ole, b) apoptosis with Ole, c) viability with PO and d) apoptosis with PO after co-treatment with palmitate (PA) and compound C (CC). Data are expressed as mean±SEM; n = 3–5 independent experiments; *p<0.05 vs control.