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Hypercholesterolaemic Serum Increases the Permeability of Endothelial Cells through Zonula Occludens-1 with Phosphatidylinositol 3-Kinase Signaling Pathway
Purpose. Hypercholesterolemia and tight junctions play important roles in atherosclerosis. But the relationship between these two factors is unclear. In the present study, we investigated whether hypercholesterolemic serum could change the permeability of endothelial cells through altering expressio...
Autores principales: | , , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2009
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2817810/ https://www.ncbi.nlm.nih.gov/pubmed/20150971 http://dx.doi.org/10.1155/2009/814979 |
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author | Bian, Chang Xu, Geng Wang, Jianan Ma, Ji Xiang, MeiXiang Chen, Peng |
author_facet | Bian, Chang Xu, Geng Wang, Jianan Ma, Ji Xiang, MeiXiang Chen, Peng |
author_sort | Bian, Chang |
collection | PubMed |
description | Purpose. Hypercholesterolemia and tight junctions play important roles in atherosclerosis. But the relationship between these two factors is unclear. In the present study, we investigated whether hypercholesterolemic serum could change the permeability of endothelial cells through altering expression and/or distribution of tight junction protein zonula occludens-1 (ZO-1). Phosphatidylinositol 3-kinase (PI3K) signaling pathway was also examined. Materials and Methods. Cultured endothelial cells were treated with different concentration levels of hypercholesterolemic serum. The expression and distribution of ZO-1, the permeability of cultured cells and the involvement of PI3K signaling pathway were measured by various methods. Results. In the present study, we found that hypercholesterolemic serum could not change the expression of ZO-1 either in mRNA or protein level. However, hypercholesterolemic serum could change the distribution of ZO-1 in cultured endothelial cells, and increase the permeability with a dose-dependent manner. When PI3K specific inhibitor wortmannin was used, the effects induced by hypercholesterolemic serum could be partly reversed. The role of PI3K signaling pathway was further confirmed by PI3K activity assay. Conclusions. Our results suggested that although hypercholesterolemic serum could not change the expression of ZO-1, it could change the distribution and increase the permeability in endothelial cells through PI3K signaling pathway. |
format | Text |
id | pubmed-2817810 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2009 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-28178102010-02-11 Hypercholesterolaemic Serum Increases the Permeability of Endothelial Cells through Zonula Occludens-1 with Phosphatidylinositol 3-Kinase Signaling Pathway Bian, Chang Xu, Geng Wang, Jianan Ma, Ji Xiang, MeiXiang Chen, Peng J Biomed Biotechnol Research Article Purpose. Hypercholesterolemia and tight junctions play important roles in atherosclerosis. But the relationship between these two factors is unclear. In the present study, we investigated whether hypercholesterolemic serum could change the permeability of endothelial cells through altering expression and/or distribution of tight junction protein zonula occludens-1 (ZO-1). Phosphatidylinositol 3-kinase (PI3K) signaling pathway was also examined. Materials and Methods. Cultured endothelial cells were treated with different concentration levels of hypercholesterolemic serum. The expression and distribution of ZO-1, the permeability of cultured cells and the involvement of PI3K signaling pathway were measured by various methods. Results. In the present study, we found that hypercholesterolemic serum could not change the expression of ZO-1 either in mRNA or protein level. However, hypercholesterolemic serum could change the distribution of ZO-1 in cultured endothelial cells, and increase the permeability with a dose-dependent manner. When PI3K specific inhibitor wortmannin was used, the effects induced by hypercholesterolemic serum could be partly reversed. The role of PI3K signaling pathway was further confirmed by PI3K activity assay. Conclusions. Our results suggested that although hypercholesterolemic serum could not change the expression of ZO-1, it could change the distribution and increase the permeability in endothelial cells through PI3K signaling pathway. Hindawi Publishing Corporation 2009 2010-01-27 /pmc/articles/PMC2817810/ /pubmed/20150971 http://dx.doi.org/10.1155/2009/814979 Text en Copyright © 2009 Chang Bian et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Bian, Chang Xu, Geng Wang, Jianan Ma, Ji Xiang, MeiXiang Chen, Peng Hypercholesterolaemic Serum Increases the Permeability of Endothelial Cells through Zonula Occludens-1 with Phosphatidylinositol 3-Kinase Signaling Pathway |
title | Hypercholesterolaemic Serum Increases the Permeability of Endothelial Cells through Zonula Occludens-1 with Phosphatidylinositol 3-Kinase Signaling Pathway |
title_full | Hypercholesterolaemic Serum Increases the Permeability of Endothelial Cells through Zonula Occludens-1 with Phosphatidylinositol 3-Kinase Signaling Pathway |
title_fullStr | Hypercholesterolaemic Serum Increases the Permeability of Endothelial Cells through Zonula Occludens-1 with Phosphatidylinositol 3-Kinase Signaling Pathway |
title_full_unstemmed | Hypercholesterolaemic Serum Increases the Permeability of Endothelial Cells through Zonula Occludens-1 with Phosphatidylinositol 3-Kinase Signaling Pathway |
title_short | Hypercholesterolaemic Serum Increases the Permeability of Endothelial Cells through Zonula Occludens-1 with Phosphatidylinositol 3-Kinase Signaling Pathway |
title_sort | hypercholesterolaemic serum increases the permeability of endothelial cells through zonula occludens-1 with phosphatidylinositol 3-kinase signaling pathway |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2817810/ https://www.ncbi.nlm.nih.gov/pubmed/20150971 http://dx.doi.org/10.1155/2009/814979 |
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