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首页> 外文期刊>The Korean Journal of Physiology & Pharmacology >Murrayafoline A Induces a G0/G1-Phase Arrest in Platelet-Derived Growth Factor-Stimulated Vascular Smooth Muscle Cells
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Murrayafoline A Induces a G0/G1-Phase Arrest in Platelet-Derived Growth Factor-Stimulated Vascular Smooth Muscle Cells

机译：Murrayafoline A在血小板衍生的生长因子刺激的血管平滑肌细胞中诱导G0 / G1期阻滞

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The increased potential for vascular smooth muscle cell (VSMC) growth is a key abnormality in the development of atherosclerosis and post-angioplasty restenosis. Abnormally high activity of platelet-derived growth factor (PDGF) is believed to play a central role in the etiology of these pathophysiological situations. Here, we investigated the anti-proliferative effects and possible mechanism(s) of murrayafoline A, a carbazole alkaloid isolated from Glycosmis stenocarpa Guillamin (Rutaceae), on PDGF-BB-stimulated VSMCs. Murrayafoline A inhibited the PDGF-BB-stimulated proliferation of VSMCs in a concentration-dependent manner, as measured using a non-radioactive colorimetric WST-1 assay and direct cell counting. Furthermore, murrayafoline A suppressed the PDGF-BB-stimulated progression through G0/G1 to S phase of the cell cycle, as measured by [3H]-thymidine incorporation assay and cell cycle progression analysis. This anti-proliferative action of murrayafoline A, arresting cell cycle progression at G0/G1 phase in PDGF-BB-stimulated VSMCs, was mediated via down-regulation of the expression of cyclin D1, cyclin E, cyclin-dependent kinase (CDK)2, CDK4, and proliferating cell nuclear antigen (PCNA), and the phosphorylation of retinoblastoma protein (pRb). These results indicate that murrayafoline A may be useful in preventing the progression of vascular complications such as restenosis after percutaneous transluminal coronary angioplasty and atherosclerosis.
机译：血管平滑肌细胞（VSMC）增长的潜力增加是动脉粥样硬化和血管成形术后再狭窄发展的关键异常。血小板源性生长因子（PDGF）异常高活性被认为在这些病理生理情况的病因中起着核心作用。在这里，我们研究了从聚乙二醇糖衣藻Guillamin（芸苔科）分离得到的咔唑生物碱—尿嘧啶A对PDGF-BB刺激的VSMC的抗增殖作用和可能的机制。如使用非放射性比色法WST-1分析和直接细胞计数所测量的，Murrayafoline A以浓度依赖性方式抑制PDGF-BB刺激的VSMC增殖。此外，如[ 3 所测量，墨瑞福林A抑制了PDGF-BB刺激的细胞周期从G 0 / G 1 到S期的进展。 sup> H]-胸苷掺入试验和细胞周期进程分析。 Murrayafoline A的这种抗增殖作用（通过抑制PDGF-BB刺激的VSMC中G 0 / G 1 期的细胞周期进程而停止）是通过下调其介导的。细胞周期蛋白D1，细胞周期蛋白E，细胞周期蛋白依赖性激酶（CDK）2，CDK4和增殖细胞核抗原（PCNA）的表达，以及成视网膜细胞瘤蛋白（pRb）的磷酸化。这些结果表明，墨瑞茶碱A可用于预防血管并发症的进展，例如经皮腔内冠状动脉成形术和动脉粥样硬化后的再狭窄。

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