首页|脂多糖诱导血管内皮细胞分泌的细胞外基质调节人肝实质细胞紧密连接蛋白表达的研究

脂多糖诱导血管内皮细胞分泌的细胞外基质调节人肝实质细胞紧密连接蛋白表达的研究

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该文分析脂多糖诱导人血管内皮细胞去分化促进细胞外基质分泌增加,调节人肝实质细胞紧密连接蛋白表达的作用.利用脂多糖诱导体外培养人脐静脉内皮细胞72 h后,分析内皮细胞特征以及分泌的细胞外基质成分表达及超微结构变化;将人肝实质细胞接种于脂多糖或对照处理的内皮细胞分泌的基质上培养72 h后,分析肝实质细胞中紧密连接蛋白、整合素及DNA甲基化及羟甲基化的变化.结果表明,脂多糖诱导人脐带静脉内皮细胞去分化,以及分泌的细胞外基质成分组成及结构发生变化;脂多糖诱导内皮细胞分泌的基质下调人肝实质细胞中紧密连接蛋白Claudin 1和整合素a5蛋白及DNA羟甲基化的水平.研究表明,受损血管内皮细胞分泌的细胞外基质抑制人肝实质细胞紧密连接蛋白Claudin 1的表达.
Research on the Endothelial Cell-Derived Matrix Induced by Lipopolysaccharide Regulates the Tight Junction Protein Expression in Human Hepatocytes
This study was to analyze the dedifferentiation of human vascular ECs(endothelial cells)and the increased extracellular matrix secretion induced by LPS(lipopolysaccharide).The regulated effect and mechanism of the EC matrix(endothelial cell-derived extracellular matrix)induced by LPS on the expres-sion of tight junction protein in human hepatocytes were study.The characteristics of endothelial cells,the components and ultrastructural changes of EC matrix were analyzed in human umbilical vein endothelial cells treated with control or LPS for 72 h.The changes of tight junction protein,integrin and DNA methylation and hydroxymethylation in human hepatocytes were analyzed after 72 h of culture on the control-EC matrix or LPS-EC matrix.LPS induced the dedifferentiation of human umbilical vein endothelial cells,and promoted the change of the composition and structure of extracellular matrix secreted by endothelial cells.LPS-EC matrix down-regulated the protein levels of Claudin 1 and integrin α5 proteins and DNA hydroxymethylation in human hepatocytes.This study indicated that the injury of vascular endothelial cell affected the tight junction protein in human hepatocytes.

vascular endothelial cellsextracellular matrixdedifferentiationhepatocytestight junction

李卫红、马悦佼、贺旭、王梓祎、郭昕悦、张海燕

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首都医科大学基础医学院基础医学国家级实验教学中心,北京 100069

首都医科大学基础医学院细胞生物学系,北京 100069

血管内皮细胞 细胞外基质 去分化 肝实质细胞 紧密连接

国家自然科学基金

81770616

2024

中国细胞生物学学报
中国科学院上海生命科学研究院,生物化学与细胞生物学研究所,中国细胞生物学学会

中国细胞生物学学报

CSTPCD
影响因子:0.554
ISSN:1674-7666
年,卷(期):2024.46(5)
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