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- W2009805438 abstract "<h3>Objectives</h3> Proliferation of vascular smooth muscle cells (VSMCs) participates in the pathogenesis and development of cardiovascular diseases, including essential hypertension and atherosclerosis. Our previous study found that stimulation of D<sub>1</sub>-like dopamine receptors inhibited insulin-induced proliferation of VSMCs. Insulin-like growth factor-1 (IGF-1) and insulin share similar structure and biological effect. However, whether or not there is any effect of D<sub>1</sub>-like receptors on IGF-1-induced proliferation of VSMCs is not known. Therefore, we investigated the inhibitory effect of D<sub>1</sub>-like dopamine receptors on the IGF-1-induced VSMCs proliferation in this study. <h3>Methods</h3> VSMC proliferation was determined by [<sup>3</sup>H]-thymidinein corporation, the uptake of 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay and cell number. Phosphorylated/non-phosphorylated IGF-1 receptor, Akt, mTOR and p70S6K expressions were determined by immunoblotting. The oligodeoxynucleotides were transfected to A10 cells to identify the effect of D<sub>1 </sub>and D<sub>5 </sub>receptors respectively. <h3>Results</h3> IGF-1 increased the proliferation of VSMCs, while in the presence of fenoldopam, IGF-1 mediated stimulatory effect was reduced. Use of either the antisense for D<sub>1</sub> or D<sub>5</sub> receptor partially inhibited the fenoldopam-induced anti-proliferation effect of VSMCs. Use of both D<sub>1</sub> andD<sub>5</sub> receptor antisenses completely blocked the inhibitory effect of fenoldopam. In the presence of PI3k and mTOR inhibitors, the IGF-1 mediated proliferation of VSMCs was blocked. Moreover, IGF-1 increased the phosphorylation of PI3k and mTOR. The inhibitory effect of fenoldopam on VSMC proliferation might be due to the inhibition of IGF-1 receptor expression and IGF-1 phosphorylation, since in the presence offenoldopam, the stimulatory effect of IGF-1 on phosphorylation of IGF-1 receptor, PI3k and mTOR is reduced, the IGF-1 receptor expression was reducedin A10 cells. <h3>Conclusions</h3> Activation of the D<sub>1</sub>-like receptors suppressed the proliferative effect of IGF-1 in A10 cells via the inhibition of the IGF-1R/Akt/mTOR/p70S6K pathway." @default.
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- W2009805438 date "2013-08-01" @default.
- W2009805438 modified "2023-10-16" @default.
- W2009805438 title "GW24-e2208 Dopamine D1-like receptors suppress proliferation of vascular smooth muscle cell induced by insulin-like growth factor-1" @default.
- W2009805438 doi "https://doi.org/10.1136/heartjnl-2013-304613.171" @default.
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