Ceramide Mediates Vascular Dysfunction in Diet-Induced Obesity by PP2A-Mediated Dephosphorylation of the eNOS-Akt Complex

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FIG. 4.
FIG. 4.

Arterial function in isolated arteries from wild-type and des1+/− mice. Aorta from 10 C57Bl/6 mice were incubated with vehicle (veh), palmitate (pal), or pal + myriocin (myr). A: Pal-induced ceramide accumulation. B: EDR assessed in four femoral artery segments from the same 10 mice. Of these four segments, two were incubated with pal for 3 h while two were incubated with pal + myr for 3 h. C: EIR post pal ± myr treatment. D: Ceramide content in aorta from 6 des1+/+ and des1+/− mice after treatment with veh or pal. E: EDR in vessels from des1+/+ and des1+/− before and after 3-h pal treatment. F: EIR post pal in both genotypes. G: p-eNOS Ser1177 to total eNOS in aorta from wild-type mice (lanes 1–3) and in aorta from des1+/− mice (lanes 4–5) treated with or without pal (n = 5 segments per treatment). Representative blot (upper) and mean densitometry (lower). *P < 0.05 pre vs. post pal incubation. Results represent mean ± SEM.

This Article

  1. Diabetes vol. 61 no. 7 1848-1859