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

Overview of attention for article published in Lipids in Health and Disease, January 2017
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Title
Myeloperoxidase-oxidized high density lipoprotein impairs atherosclerotic plaque stability by inhibiting smooth muscle cell migration
Published in
Lipids in Health and Disease, January 2017
DOI 10.1186/s12944-016-0388-z
Pubmed ID
Authors

Boda Zhou, Lingyun Zu, Yong Chen, Xilong Zheng, Yuhui Wang, Bing Pan, Min Dong, Enchen Zhou, Mingming Zhao, Youyi Zhang, Lemin Zheng, Wei Gao

Abstract

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. 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. 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. 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.

Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 35 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Netherlands 1 3%
Germany 1 3%
Unknown 33 94%

Demographic breakdown

Readers by professional status Count As %
Researcher 5 14%
Student > Doctoral Student 4 11%
Student > Bachelor 4 11%
Student > Master 4 11%
Student > Ph. D. Student 4 11%
Other 6 17%
Unknown 8 23%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 10 29%
Medicine and Dentistry 7 20%
Nursing and Health Professions 2 6%
Pharmacology, Toxicology and Pharmaceutical Science 1 3%
Environmental Science 1 3%
Other 4 11%
Unknown 10 29%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 01 November 2017.
All research outputs
#20,451,228
of 23,007,053 outputs
Outputs from Lipids in Health and Disease
#1,207
of 1,457 outputs
Outputs of similar age
#357,123
of 421,999 outputs
Outputs of similar age from Lipids in Health and Disease
#26
of 33 outputs
Altmetric has tracked 23,007,053 research outputs across all sources so far. This one is in the 1st percentile – i.e., 1% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,457 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 8.1. This one is in the 1st percentile – i.e., 1% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 421,999 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 1st percentile – i.e., 1% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 33 others from the same source and published within six weeks on either side of this one. This one is in the 1st percentile – i.e., 1% of its contemporaries scored the same or lower than it.