血管内皮细胞增殖过程中碘离子与MEK1表达及磷酸化关系的研究

2015-10-27胡琳祖茂衡华浅近王丹

介入放射学杂志 2015年2期

胡琳，祖茂衡，华浅近，王丹

胡琳，祖茂衡，华浅近，王丹

目的研究血管内皮细胞（VEC）增殖过程中碘离子（I-）与丝裂原活化蛋白激酶1（MEK1）表达及其磷酸化的关系，探讨高碘促VEC增殖效应的作用通路。方法①将体外培养的VEC分为空白对照组和不同碘离子浓度的实验组。②采用蛋白质印迹技术（Western blot）检测不同碘离子浓度培养环境中MEK1蛋白表达量及磷酸化水平。结果①在300 μg/L碘离子浓度组，MEK1蛋白相对表达量高于其他组（P＜0.05）。②500 μg/L、1 000 μg/L碘离子浓度可促进MEK1（Ser298位点）磷酸化水平上调（P＜0.05）。③各实验组MEK1（Thr286位点）磷酸化水平下调（P＜0.05）。结论碘促VEC增殖可能与胞外信号调节激酶（ERK）通路的激活有关。

布加综合征；血管内皮细胞；碘离子

【Abstract】ObjectiveTo investigate the relationship between iodine ion and the expression of both MEK1 and its phosphorylation during the course of vascular endothelial cell（VEC）proliferation，and to explore the pathway of the promoting effect of iodine ion on VEC proliferation.Methods①The vascular endothelial cells cultured in vitro were divided into the control group（without any treatment）and four KI groups（treated with 100 μg/L KI，300 μg/L KI，500 μg/L K and 1 000 μg/L KI，respectively）.②The effects of iodine ion concentration（100 μg/L，300 μg/L，500 μg/L and 1 000 μg/L，respectively）on the expression of MEK1 and its phosphorylation were determined using Western Blot method.Results①The expression of MEK1 in 300 μg/L KI group was higher than that in other groups（P＜0.05）.②The MEK1 phosphorylation levels at Ser298 site in iodine ion concentration of 500 μg/L and 1 000 μg/L groups were significantly increased（P＜0.05）.③The MEK1 phosphorylation levels at Thr286 site in all different iodine ion concentration groups were significantly decreased（P＜0.05）.ConclusionThe promotion effect of iodine ion on vascular endothelial cell proliferation is related to the activation of extracellular signal-regulated kinase（ERK）signal transduction.（J Intervent Radiol，2015，24：150-153）

【Key words】Budd-Chiari syndrome；vascular endothelial cell；iodine ion

我国布加综合征（Budd-Chiari syndrome，BCS）以下腔静脉隔膜阻塞型（membranous obstruction ofthe inferior vene cava，MOVC）为主，其特征是下腔静脉和（或）肝静脉开口处隔膜形成。病理学研究发现隔膜组织主要由血管内皮和纤维组织构成［1-2］。同时流行病学研究显示该型患者分布与水源性高碘地区分布相符［3］。针对碘离子（I-）与血管内皮细胞（VEC）增殖的关系，研究显示碘不促进VEC合成血管内皮生长因子（VEGF）［4］，且高碘环境未诱导VEGF受体（VEGFR）与VEC增殖有关的位点磷酸化改变［5］。但细胞增殖检测显示碘促VEC增殖可能与MEK1激活有关［6］，提示高碘促VEC增殖效应可能发生于细胞质。

本研究在体外用不同浓度I-培养VEC，检测MEK1的表达及调控增殖相关位点Ser298、Thr286的磷酸化水平，探讨高碘促VEC增殖效应的作用通路。