Abstract:
:Oxidized lipoprotein(a) (oxLp(a)) is a more potent marker of atherogenesis than native Lp(a). However, the molecular mechanisms of oxLp(a) activity are not clear. Reactive oxygen species (ROS) have recently been suggested as acting as intracellular second messengers. In this study, the effects of oxLp(a) on endothelial cell monolayer permeability and the role of reactive oxygen species (ROS) generation in these effects were investigated. Our results showed that oxLp(a) inhibited desmoglein-1 (DSG1) and desmocollin-2 (DSC2) expression at both mRNA and protein levels in a dose- and time-dependent manner, and increased the generation of cellular ROS. Down-regulation of DSG1 and DSC2 was strengthened by pretreatment with H₂O₂ and attenuated by superoxide dismutase (SOD) treatment. Furthermore, oxLp(a) increased endothelial cell monolayer permeability, and this effect was enhanced by H₂O₂ and blunted by SOD. Taken together, these results demonstrate that oxLp(a) increases endothelial cell monolayer permeability, which is mediated at least in part via ROS generation.
journal_name
Lipidsjournal_title
Lipidsauthors
Wei DH,Zhang XL,Wang R,Zeng JF,Zhang K,Yang J,Li S,Lin XL,Jiang ZS,Wang GX,Wang Zdoi
10.1007/s11745-013-3795-1subject
Has Abstractpub_date
2013-06-01 00:00:00pages
579-86issue
6eissn
0024-4201issn
1558-9307journal_volume
48pub_type
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