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High-density lipoproteins suppress Aβ-induced PBMC adhesion to human endothelial cells in bioengineered vessels and in monoculture

Overview of attention for article published in Molecular Neurodegeneration, August 2017
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About this Attention Score

  • In the top 25% of all research outputs scored by Altmetric
  • Among the highest-scoring outputs from this source (#41 of 596)
  • High Attention Score compared to outputs of the same age (88th percentile)
  • High Attention Score compared to outputs of the same age and source (80th percentile)

Mentioned by

blogs
1 blog
twitter
17 tweeters
facebook
1 Facebook page

Citations

dimensions_citation
19 Dimensions

Readers on

mendeley
27 Mendeley
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Title
High-density lipoproteins suppress Aβ-induced PBMC adhesion to human endothelial cells in bioengineered vessels and in monoculture
Published in
Molecular Neurodegeneration, August 2017
DOI 10.1186/s13024-017-0201-0
Pubmed ID
Authors

Jérôme Robert, Emily B. Button, Sophie Stukas, Guilaine K. Boyce, Ebrima Gibbs, Catherine M. Cowan, Megan Gilmour, Wai Hang Cheng, Sonja K. Soo, Brian Yuen, Arvin Bahrabadi, Kevin Kang, Iva Kulic, Gordon Francis, Neil Cashman, Cheryl L. Wellington

Abstract

Alzheimer's Disease (AD), characterized by accumulation of beta-amyloid (Aβ) plaques in the brain, can be caused by age-related failures to clear Aβ from the brain through pathways that involve the cerebrovasculature. Vascular risk factors are known to increase AD risk, but less is known about potential protective factors. We hypothesize that high-density lipoproteins (HDL) may protect against AD, as HDL have vasoprotective properties that are well described for peripheral vessels. Epidemiological studies suggest that HDL is associated with reduced AD risk, and animal model studies support a beneficial role for HDL in selectively reducing cerebrovascular amyloid deposition and neuroinflammation. However, the mechanism by which HDL may protect the cerebrovascular endothelium in the context of AD is not understood. We used peripheral blood mononuclear cell adhesion assays in both a highly novel three dimensional (3D) biomimetic model of the human vasculature composed of primary human endothelial cells (EC) and smooth muscle cells cultured under flow conditions, as well as in monolayer cultures of ECs, to study how HDL protects ECs from the detrimental effects of Aβ. Following Aβ addition to the abluminal (brain) side of the vessel, we demonstrate that HDL circulated within the lumen attenuates monocyte adhesion to ECs in this biofidelic vascular model. The mechanism by which HDL suppresses Aβ-mediated monocyte adhesion to ECs was investigated using monotypic EC cultures. We show that HDL reduces Aβ-induced PBMC adhesion to ECs independent of nitric oxide (NO) production, miR-233 and changes in adhesion molecule expression. Rather, HDL acts through scavenger receptor (SR)-BI to block Aβ uptake into ECs and, in cell-free assays, can maintain Aβ in a soluble state. We confirm the role of SR-BI in our bioengineered human vessel. Our results define a novel activity of HDL that suppresses Aβ-mediated monocyte adhesion to the cerebrovascular endothelium.

Twitter Demographics

The data shown below were collected from the profiles of 17 tweeters who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 27 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 27 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 6 22%
Student > Master 6 22%
Student > Bachelor 5 19%
Researcher 4 15%
Student > Doctoral Student 1 4%
Other 3 11%
Unknown 2 7%
Readers by discipline Count As %
Neuroscience 6 22%
Biochemistry, Genetics and Molecular Biology 5 19%
Agricultural and Biological Sciences 4 15%
Engineering 2 7%
Immunology and Microbiology 2 7%
Other 4 15%
Unknown 4 15%

Attention Score in Context

This research output has an Altmetric Attention Score of 19. 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 11 November 2017.
All research outputs
#925,875
of 14,157,352 outputs
Outputs from Molecular Neurodegeneration
#41
of 596 outputs
Outputs of similar age
#29,802
of 269,153 outputs
Outputs of similar age from Molecular Neurodegeneration
#1
of 5 outputs
Altmetric has tracked 14,157,352 research outputs across all sources so far. Compared to these this one has done particularly well and is in the 93rd percentile: it's in the top 10% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 596 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 8.9. This one has done particularly well, scoring higher than 93% of its peers.
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 269,153 tracked outputs that were published within six weeks on either side of this one in any source. This one has done well, scoring higher than 88% of its contemporaries.
We're also able to compare this research output to 5 others from the same source and published within six weeks on either side of this one. This one has scored higher than all of them