Abstract
Vascular smooth muscle cell (VSMC) proliferation plays a central role in the pathogenesis of obesity-related atherosclerosis. The molecular mechanism of GA on oleic acid (OA)-induced proliferation of vascular smooth muscle cell is evaluated. Cells were treated with OA (150 μM), or co-treated with OA and GA (10-30 μM) for 48 h, MTT assay was performed for proliferation. Using flow cytometry analysis, the GA-treated cells caused an increase in G2/M phase. A decrease in cyclin B1 and cyclin-dependent kinase 1 (cdc2) and increase in kip/p27 and cip1/p21 were found by western blotting. Additional mechanistic studies showed that GA induced the activation of AMP-activated protein kinase (AMPK) and eNOS and the inhibition of fatty acid synthase (FAS) after stimulation with OA. Furthermore, the addition of compound C, a specific inhibitor of AMPK, reduced the activation of GA-mediated eNOS and NO production and increased the proliferation of cells. Inhibition of NOS by L-NAME had no further effect on VSMC proliferation. The present results indicate that GA was an effected and anti-atherogenic agent in VSMC. It attenuates cell cycle progression via AMPKmediated eNOS activation, which results in the production of NO and prevents atherosclerosis.
Keywords: Vascular smooth muscle cells, proliferation, gallic acid, oleic acid, AMP-activated protein kinase (AMPK), eNOS.
Current Medicinal Chemistry
Title:Gallic Acid Attenuates Oleic Acid-induced Proliferation of Vascular Smooth Muscle Cell Through Regulation of AMPK-eNOS-FAS Signaling
Volume: 20 Issue: 31
Author(s): Ting-Tsz Ou, Ming-Cheng Lin, Cheng-Hsun Wu, Wea-Lung Lin and Chau-Jong Wang
Affiliation:
Keywords: Vascular smooth muscle cells, proliferation, gallic acid, oleic acid, AMP-activated protein kinase (AMPK), eNOS.
Abstract: Vascular smooth muscle cell (VSMC) proliferation plays a central role in the pathogenesis of obesity-related atherosclerosis. The molecular mechanism of GA on oleic acid (OA)-induced proliferation of vascular smooth muscle cell is evaluated. Cells were treated with OA (150 μM), or co-treated with OA and GA (10-30 μM) for 48 h, MTT assay was performed for proliferation. Using flow cytometry analysis, the GA-treated cells caused an increase in G2/M phase. A decrease in cyclin B1 and cyclin-dependent kinase 1 (cdc2) and increase in kip/p27 and cip1/p21 were found by western blotting. Additional mechanistic studies showed that GA induced the activation of AMP-activated protein kinase (AMPK) and eNOS and the inhibition of fatty acid synthase (FAS) after stimulation with OA. Furthermore, the addition of compound C, a specific inhibitor of AMPK, reduced the activation of GA-mediated eNOS and NO production and increased the proliferation of cells. Inhibition of NOS by L-NAME had no further effect on VSMC proliferation. The present results indicate that GA was an effected and anti-atherogenic agent in VSMC. It attenuates cell cycle progression via AMPKmediated eNOS activation, which results in the production of NO and prevents atherosclerosis.
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Ou Ting-Tsz, Lin Ming-Cheng, Wu Cheng-Hsun, Lin Wea-Lung and Wang Chau-Jong, Gallic Acid Attenuates Oleic Acid-induced Proliferation of Vascular Smooth Muscle Cell Through Regulation of AMPK-eNOS-FAS Signaling, Current Medicinal Chemistry 2013; 20 (31) . https://dx.doi.org/10.2174/09298673113209990175
DOI https://dx.doi.org/10.2174/09298673113209990175 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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