Abstract：
:There is growing evidence that exposure to persistent organic pollutants (POPs) is statistically associated with incidence of cardiovascular disease (CVD) or its risk factors. Decarbromodiphenyl ether (BDE-209) is a new POP which exists extensively in human tissues, but its potential effects on CVD have so far received less focus. The adhesion of circulating monocytes to endothelial cells is one of the critical underlying steps in the initiation and development of CVD. In the present study, we investigated the effect of BDE-209 on the adhesion of THP-1 monocytes to human aortic endothelial cells (HAECs) and identified the molecular mechanisms involved. Our results showed that 6.25, 12.5 and 25 µM of BDE-209 exposures caused significant increases in monocyte-endothelial cell adhesion, in a dose-dependent manner. Mechanistically, BDE-209 exposure increased the expression of intercellular adhesion molecule-1 (ICAM-1). Moreover, the up-regulation of ICAM-1 was accompanied by a decrease in the expression of microRNA-141 (miR-141). Furthermore, the up-regulation of ICAM-1 and the increased adhesion induced by BDE-209 could be reversed by miR-141 supplement. Taken together, our results show that BDE-209 potentiates monocyte-endothelial cell interaction via miR-141/ICAM-1 pathway in HAECs.
journal_name
Environ Resjournal_title
Environmental researchauthors
Zhi H,Wu JP,Lu LM,Zhang XM,Chen XY,Wu SK,Tao J,Mai BXdoi
10.1016/j.envres.2018.10.035subject
Has Abstractpub_date
2019-02-01 00:00:00pages
62-71eissn
0013-9351issn
1096-0953pii
S0013-9351(18)30567-Xjournal_volume
169pub_type
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journal_title：Environmental research
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pub_type： 杂志文章
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pub_type： 杂志文章
doi：10.1006/enrs.1999.4014
更新日期：2000-06-01 00:00:00
