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首页> 外文期刊>Journal of Cellular Physiology >Modulation of vascular smooth muscle cell growth by magnesium-role of mitogen-activated protein kinases.
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Modulation of vascular smooth muscle cell growth by magnesium-role of mitogen-activated protein kinases.

机译：调节血管平滑肌细胞的增长magnesium-role增殖作用的蛋白质激酶。

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We tested the hypothesis that Mg(2+) influences growth of vascular smooth muscle cells (VSMCs) by modulating cell cycle activation through mitogen-activated protein (MAP) kinase-dependent pathways. Rat VSMCs were grown in culture medium containing normal Mg(2+) (1.02 mmol/L, control) and increasing concentrations of Mg(2+) (2-4 mmol/L) for 1-8 days. Effects of varying extracellular Mg(2+) concentration ([Mg(2+)](e)) on intracellular free Mg(2+) concentration ([Mg(2+)](i)) were assessed using mag-fura. Growth actions of Mg(2+) were evaluated by measuring cell cycle activation, DNA synthesis, and protein synthesis. Expression of cell cycle promoters, cyclin D1, cyclin E, Cdk2, and Cdk4 was assessed by immunoblotting. Phosphorylation of cell cycle inhibitors p21(cip1) and p27(kip1) and MAP kinases, ERK1/2, p38MAP kinase, and JNK was evaluated using phospho-specific antibodies. [Mg(2+)](i) increased in a dose-dependent manner in response to increasing [Mg(2+)](e). These effects were evident within 2 days and maximal responses were obtained after 6 days. High [Mg(2+)](e) induced cell cycle activation with a lower proportion of cells in G(1) phase (75 +/- 1.0%) and a higher fraction of cells in S phase (12 +/- 0.7%) versus control (G(1), 88.5 +/- 1.4%; S, 6.8 +/- 1.2%; P < 0.05). This was associated with increased protein content of cyclin D1 and Cdk4 and decreased activation of p21(cip1) and p27(kip1). In cells exposed to 2 mmol/L Mg(2+), DNA and protein synthesis was increased approximately threefold. Phosphorylation of MEK1/2 and ERK1/2 was enhanced two to threefold in cells grown in 2 mmol/L Mg(2+). These effects were rapid, occurring within 2 days. Phosphorylation of MEK3/6, p38 MAP kinase, and JNK was unaltered by increasing [Mg2](e). PD98059 (10(-5) mol/L), specific MEK1/2 inhibitor, but not SB202190 (10(-5) mol/L) (specific p38 MAP kinase inhibitor), attenuated Mg(2+)-induced growth actions. These data demonstrate the novel findings that cell cycle activation and growth regulation by Mg(2+) occurs via ERK1/2-dependent, p38 MAP kinase-independent pathways. J. Cell. Physiol. 197: 326-335, 2003Copyright 2003 Wiley-Liss, Inc.
机译：我们测试的假设镁(2 +)的影响血管平滑肌细胞(VSMCs)调节细胞周期激活增殖kinase-dependent(地图)通路。包含正常毫克(2 +)(1.02更易/ L,控制)和增加浓度的镁(2 +)(2 - 4更易/ L) 1 - 8天。胞外镁(2 +)浓度((镁(2 +))(e))胞内自由镁(2 +)浓度(镁(2 +))((我))使用mag-fura进行评估。增长的行为毫克(2 +)进行评估测量细胞周期激活、DNA合成、和蛋白质合成。启动子,细胞周期蛋白D1、细胞周期素E、Cdk2、到被免疫印迹评估。细胞周期抑制剂p21和p27 cip1 (kip1)MAP激酶,ERK1/2 p38MAP激酶和物评估使用phospho-specific抗体。(镁(2 +))(i)增加剂量依赖性的方式为了增加(镁(2 +))(e)。在2天,最大的影响是明显的反应后得到6天。(镁(2 +))(e)诱导细胞周期激活的低比例的细胞G(75 + / -(1)阶段1.0%)和更高的分数在S期的细胞(12 + / - 0.7%)和控制(G (1), 88.5 + / -1.4%;与蛋白质含量的增加有关细胞周期蛋白D1到和激活降低p21和p27 cip1 (kip1)。更易与Mg / L (2 +), DNA和蛋白质合成增加了约3倍。磷酸化MEK1/2和ERK1/2增强在细胞生长在2两到三倍更易与L镁(2 +)。在2天之内。激酶,物的增加[Mg2] (e)。抑制剂,但不是SB202190 (10 (5) mol / L)(具体p38激酶抑制剂地图),减毒镁(2 +)全身的生长行为。展示小说发现细胞周期激活和生长调节镁(2 +)发生通过ERK1/2-dependent p38 kinase-independent地图通路。2003年版权2003年Wiley-Liss公司。

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