کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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1990342 | 1540679 | 2012 | 6 صفحه PDF | دانلود رایگان |

Smooth muscle cell (SMC) migration is a major and complex feature of atherosclerosis and restenosis. N-3 long-chain polyunsaturated fatty acids (LCPUFAs) affect SMC migration; however, the mechanisms involved are unclear. This study investigated the effects of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on the MEK/ERK pathway and urokinase plasminogen activator receptor (uPAR) in relation to SMC migration.Transwell migration assays revealed that both EPA and DHA decreased cell migration. Western blotting and real-time reverse transcription polymerase chain reaction showed that n-3 LCPUFAs decreased uPAR expression, but not urokinase plasminogen activator (uPA) expression, without changing plasmin and uPA activity. DHA also inhibited the activation of the MEK/ERK signaling pathway, whereas EPA switched the SMC phenotype from synthetic to contractile. siRNA technology targeting uPAR expression showed that decreased uPAR led to a significant decrease in migration, demonstrating the role of uPAR on SMC migration. We also showed that MEK/ERK pathway activation was involved in the regulation of uPAR gene expression in SMCs.Our results suggest that n-3 LCPUFAs decrease SMC migration through the inhibition of uPAR expression, with DHA affecting its expression via the modulation of MEK/ERK signaling pathway, while EPA induces a change in SMC phenotype. This could represent another means by which to explain how n-3 LCPUFAs exert their preventive properties against atherosclerosis.
Journal: The Journal of Nutritional Biochemistry - Volume 23, Issue 11, November 2012, Pages 1378–1383