Key result
oxLDL cuts endothelial eNOS protein levels ~74%, with smaller reductions from LDL and glucose.
Hyperglycemia and elevated LDL/oxLDL decrease eNOS protein levels in endothelial cells, whereas elastin-derived peptides do not, suggesting their proatherogenic properties are independent of eNOS.
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Cell culture findings warrant no practice change; they leave open eNOS-independent atherogenic roles for elastin peptides.
Endothelial dysfunction plays an important role in the development of atherosclerosis. Elastin-derived peptides (EDP), hyperglycemia, hypercholesterolemia and oxidized LDL have a proven proatherosclerotic potential. Nitric oxide generated by endothelial nitric oxide synthase (eNOS; EC 1.14.13.39) is an important vasorelaxant. Here we studied the influence of those proatherosclerotic factors on eNOS gene and protein expression in artery-derived endothelial cells. Human umbilical artery endothelial cells (HUAEC) were incubated with or without: glucose (270 mg/dl), LDL (200 mg/dl), oxidized LDL (oxLDL 25 mg/dl) or κ-elastin (0.5 and 2.5 µg/ml). Gene expression was assessed by real time RT-PCR, whilst the eNOS protein by ELISA. In cells incubated with 2.5 µg/ml of κ-elastin, a 31 % increase of eNOS mRNA expression was observed, but the protein level remained unchanged. OxLDL, LDL and glucose decreased the eNOS protein level by 74 %, 37 % and 29 %, respectively. OxLDL decreased eNOS mRNA by 42 %. LDL non-significantly decreased eNOS mRNA expression. An elevated glucose level did not affect the eNOS mRNA expression. Hyperglycemia and an elevated level of LDL, particularly oxLDL, decreased the level of eNOS protein in endothelial cells. As κ-elastin did not decrease the expression of eNOS gene in HUAEC, the proatherogenic properties of elastin-derived peptides are unlikely to be due to their influence on eNOS.
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Garczorz et al. (2011) studied Endothelial dysfunction / Atherosclerosis. Glucose, LDL, oxidized LDL, and κ-elastin vs. Cells incubated without these factors was evaluated on eNOS gene and protein expression. Exposure of human umbilical artery endothelial cells to oxLDL, LDL, and glucose decreased eNOS protein levels by 74%, 37%, and 29%, respectively, whereas κ-elastin did not decrease eNOS expression.
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