Microcystins Induces Vascular Inflammation in Human Umbilical Vein Endothelial Cells via Activation of NF-κB

Microcystins Induces Vascular Inflammation in Human Umbilical Vein Endothelial Cells via Activation of NF-κB

Microcystins (MCs) produced by toxic cyanobacteria cause serious water pollution and public health hazard to humans and animals. However, direct molecular mechanisms of MC-LR in vascular endothelial cells (ECs) have not been understood yet. In this study, we investigated whether MC-LR induces vascul...

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Main Authors: Jun Shi, Jie Zhou, Min Zhang
Format: Article
Language:English
Published: Hindawi Limited 2015-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2015/942159
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spelling doaj-90e2709cd9a04720b0048052370530012020-11-24T22:06:33ZengHindawi LimitedMediators of Inflammation0962-93511466-18612015-01-01201510.1155/2015/942159942159Microcystins Induces Vascular Inflammation in Human Umbilical Vein Endothelial Cells via Activation of NF-κBJun Shi0Jie Zhou1Min Zhang2Key Laboratory of Yangtze River Water Environment, College of Environmental Science and Engineering, Tongji University, Ministry of Education, Shanghai 200092, ChinaDepartment of Stomatology, Changzheng Hospital, Second Military Medical University, Shanghai 200003, ChinaDivision of Cardiology, Tongren Hospital, School of Medicine, Shanghai Jiao Tong University, 1111 Xianxia Road, Shanghai 200336, ChinaMicrocystins (MCs) produced by toxic cyanobacteria cause serious water pollution and public health hazard to humans and animals. However, direct molecular mechanisms of MC-LR in vascular endothelial cells (ECs) have not been understood yet. In this study, we investigated whether MC-LR induces vascular inflammatory process in cultured human umbilical vein endothelial cells (HUVECs). Our data demonstrated that MC-LR decreased HUVECs proliferation and tube formation and enhanced apoptosis. MC-LR also induced intracellular reactive oxygen species formation (ROS) in HUVECs. The MC-LR directly stimulated phosphorylation of NF-κB. Furthermore, MC-LR also increased cell adhesion molecules (ICAM-1 and VCAM-1) expression in HUVECs. Taken together, the present data suggested that MC-LR induced vascular inflammatory process, which may be closely related to the oxidative stress, NF-κB activation, and cell adhesion molecules expression in HUVECs. Our findings may highlight that MC-LR causes potential damage to blood vessels.http://dx.doi.org/10.1155/2015/942159
collection DOAJ
language English
format Article
sources DOAJ
author Jun Shi
Jie Zhou
Min Zhang
spellingShingle Jun Shi
Jie Zhou
Min Zhang
Microcystins Induces Vascular Inflammation in Human Umbilical Vein Endothelial Cells via Activation of NF-κB
Mediators of Inflammation
author_facet Jun Shi
Jie Zhou
Min Zhang
author_sort Jun Shi
title Microcystins Induces Vascular Inflammation in Human Umbilical Vein Endothelial Cells via Activation of NF-κB
title_short Microcystins Induces Vascular Inflammation in Human Umbilical Vein Endothelial Cells via Activation of NF-κB
title_full Microcystins Induces Vascular Inflammation in Human Umbilical Vein Endothelial Cells via Activation of NF-κB
title_fullStr Microcystins Induces Vascular Inflammation in Human Umbilical Vein Endothelial Cells via Activation of NF-κB
title_full_unstemmed Microcystins Induces Vascular Inflammation in Human Umbilical Vein Endothelial Cells via Activation of NF-κB
title_sort microcystins induces vascular inflammation in human umbilical vein endothelial cells via activation of nf-κb
publisher Hindawi Limited
series Mediators of Inflammation
issn 0962-9351
1466-1861
publishDate 2015-01-01
description Microcystins (MCs) produced by toxic cyanobacteria cause serious water pollution and public health hazard to humans and animals. However, direct molecular mechanisms of MC-LR in vascular endothelial cells (ECs) have not been understood yet. In this study, we investigated whether MC-LR induces vascular inflammatory process in cultured human umbilical vein endothelial cells (HUVECs). Our data demonstrated that MC-LR decreased HUVECs proliferation and tube formation and enhanced apoptosis. MC-LR also induced intracellular reactive oxygen species formation (ROS) in HUVECs. The MC-LR directly stimulated phosphorylation of NF-κB. Furthermore, MC-LR also increased cell adhesion molecules (ICAM-1 and VCAM-1) expression in HUVECs. Taken together, the present data suggested that MC-LR induced vascular inflammatory process, which may be closely related to the oxidative stress, NF-κB activation, and cell adhesion molecules expression in HUVECs. Our findings may highlight that MC-LR causes potential damage to blood vessels.
url http://dx.doi.org/10.1155/2015/942159
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AT jiezhou microcystinsinducesvascularinflammationinhumanumbilicalveinendothelialcellsviaactivationofnfkb
AT minzhang microcystinsinducesvascularinflammationinhumanumbilicalveinendothelialcellsviaactivationofnfkb
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