Myeloperoxidase-oxidized high density lipoprotein impairs atherosclerotic plaque stability by inhibiting smooth muscle cell migration

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dc.contributor.authorZhou, Boda
dc.contributor.authorZu, Lingyun
dc.contributor.authorChen, Yong
dc.contributor.authorZheng, Xilong
dc.contributor.authorWang, Yuhui
dc.contributor.authorPan, Bing
dc.contributor.authorDong, Min
dc.contributor.authorZhou, Enchen
dc.contributor.authorZhao, Mingming
dc.contributor.authorZhang, Youyi
dc.contributor.authorZheng, Lemin
dc.contributor.authorGao, Wei
dc.date.accessioned2018-09-26T12:05:58Z
dc.date.available2018-09-26T12:05:58Z
dc.date.issued2017-01-10
dc.date.updated2018-09-26T12:05:58Z
dc.description.abstractAbstract Background High density lipoprotein (HDL) has been proved to be a protective factor for coronary heart disease. Notably, HDL in atherosclerotic plaques can be nitrated (NO2-oxHDL) and chlorinated (Cl-oxHDL) by myeloperoxidase (MPO), likely compromising its cardiovascular protective effects. Method Here we determined the effects of NO2-oxHDL and Cl-oxHDL on SMC migration using wound healing and transwell assays, proliferation using MTT and BrdU assays, and apoptosis using Annexin-V assay in vitro, as well as on atherosclerotic plaque stability in vivo using a coratid artery collar implantation mice model. Results Our results showed that native HDL promoted SMC proliferation and migration, whereas NO2-oxHDL and Cl-oxHDL inhibited SMC migration and reduced capacity of stimulating SMC proliferation as well as migration, respectively. OxHDL had no significant influence on SMC apoptosis. In addition, we found that ERK1/2-phosphorylation was significantly lower when SMCs were incubated with NO2-oxHDL and Cl-oxHDL. Furthermore, transwell experiments showed that differences between native HDL, NO2-oxHDL and Cl-oxHDL was abolished after PD98059 (MAPK kinase inhibitor) treatment. In aortic SMCs from scavenger receptor BI (SR-BI) deficient mice, differences between migration of native HDL, NO2-oxHDL and Cl-oxHDL treated SMCs vanished, indicating SR-BI’s possible role in HDL-associated SMC migration. Importantly, NO2-oxHDL and Cl-oxHDL induced neointima formation and reduced SMC positive staining cells in atherosclerotic plaque, resulting in elevated vulnerable index of atherosclerotic plaque. Conclusion These findings implicate MPO-catalyzed oxidization of HDL may contribute to atherosclerotic plaque instability by inhibiting SMC proliferation and migration through MAPK-ERK pathway which was dependent on SR-BI.
dc.identifier.citationLipids in Health and Disease. 2017 Jan 10;16(1):3
dc.identifier.doihttps://doi.org/10.1186/s12944-016-0388-z
dc.identifier.urihttp://hdl.handle.net/1880/107963
dc.identifier.urihttps://doi.org/10.11575/PRISM/44990
dc.language.rfc3066en
dc.rights.holderThe Author(s).
dc.titleMyeloperoxidase-oxidized high density lipoprotein impairs atherosclerotic plaque stability by inhibiting smooth muscle cell migration
dc.typeJournal Article
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