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Obese  hypertensive patients with cardiovascular risk factor  clustering and increased risk for atherosclerotic disease have  increased plasma nonesterified fatty acid levels, including oleic acid  (OA), and a more active  renin-angiotensin-aldosterone system. Vascular  smooth muscle cell (VSMC) migration and proliferation participate in  the development of atherosclerotic plaque. OA and  angiotensin (Ang) II induce synergistic  mitogenic responses in VSMCs through sequential signaling  pathways dependent on the activation of protein kinase C (PKC),  oxidants (reactive oxygen species, ROS), and extracellular  signal-regulated kinase (ERK) activation. We tested the hypotheses that  (1) OA and Ang II have additive or synergistic effects on VSMC  migration and (2) PKC, ROS, and mitogen-activated protein  kinase are critical signaling molecules. OA at 100 μmol/L increases  VSMC migration 60±10% over control  (P &lt;0.001). Ang II  (10− 9 mol/L)  increases VSMC migration by 62±13% and 73% over control,  respectively (P &lt;0.01).  Coincubation of cells with OA and Ang II produces a nearly additive  increase in VSMC cell migration at 107±20%  (P &lt;0.01). Increases in VSMC  migration induced by OA alone and combined with Ang II were reduced by  PKC inhibition and downregulation. VSMC migration in response to OA  alone and with Ang II was also inhibited byN -acetyl-cysteine, MEK  inhibition, and ERK antisense. VSMC migration in response to OA alone  or combined with Ang II is dependent on activation of PKC, ROS, and ERK  activation, further raising the possibility that increased plasma  nonesterified fatty acids and an activated  renin-angiotensin-aldosterone system in  subjects with the risk factor cluster contribute to accelerated  atherosclerosis through a PKC, ROS, and ERK-dependent  signaling pathway.

Signaling Events Mediating the Additive Effects of Oleic Acid and Angiotensin II on Vascular Smooth Muscle Cell Migration