Expression of Vascular Cell Adhesion Molecule-1 on Human Pulmonary ArteryEndothelial Cells and Human Umbilical Vein Endothelial Cells Stimulated by Tumor NecrosisFactor-α, Interleukin-1β and Lipopolysaccharide
スポンサーリンク
概要
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It has been recently suggested that there is a diversity of endothelial cells (ECs) from different organs in response to cytokines and lipopolysaccharide (LPS). We examined whether there was a differential response among human pulmonary artery ECs (HPAECs) and human umbilical vein ECs (HUVECs) with regard to the expression of vascular cell adhesion molecule-1 (VCAM-1) by tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and LPS stimulation. VCAM-1 expression on these ECs stimulated by the stimulators was measured by cellular enzyme-linked immunosorbent assay (ELISA) and flow cytometric analysis. For confirmation of our use of cells as ECs, the expression of Factor VIII and CD36 were also measured by flow cytometric analysis. Factor VIII was expressed on unstimulated HPAECs and HUVECs at positive cell, 43.1% and 28.9%, respectively, but not CD36 on these ECs entirely. VCAM-1 was not expressed on unstimulated HPAECs and HUVECs. Maximal expression of VCAM-1 on these ECs was induced 6 h after stimulation by TNF-α, IL-1β and LPS at doses of 10 ng/mL, 1 ng/mL and 1 µg/mL, respectively. There was a significant difference in the maximal expression between these ECs (P < 0.05; Mann-Whitney U test). Furthermore, VCAM-1 expression by any stimulation was invariably greater on HPAECs than on HUVECs throughout the course of the experiment (P < 0.01; two-way ANOVA). Therefore, we suggested that ECs from different organs might have diversity with regard to VCAM-1 expression by TNF-α, IL-1β and LPS stimulation.
- 鳥取大学の論文
著者
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Sano Hiroyuki
Graduate School Of Science University Of Tokyo
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Sano H
Graduate School Of Science University Of Tokyo
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Sano Hiroyuki
Third Department of Internal Medicine, Faculty of Medicine, Tottori University
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- Expression of Vascular Cell Adhesion Molecule-1 on Human Pulmonary ArteryEndothelial Cells and Human Umbilical Vein Endothelial Cells Stimulated by Tumor NecrosisFactor-α, Interleukin-1β and Lipopolysaccharide