Evidence map›Paper›PMID 28476857›Full record

ArticleJournal of lipid research2017

Apolipoprotein A-II alters the proteome of human lipoproteins and enhances cholesterol efflux from ABCA1.

John T Melchior, Scott E Street, Allison B Andraski, Jeremy D Furtado, Frank M Sacks, Rebecca L Shute, Emily I Greve, Debi K Swertfeger, Hailong Li, Amy S Shah and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
5.0field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

46 citing papers in PubMed, 69 citations in OpenAlex.

  1. Trial
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  8. Apolipoprotein A (ApoA) in Neurological Disorders: Connections and Insights.International journal of molecular sciences · 2025
    Review
  9. Article
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  13. Review
  14. Understanding HDL Metabolism and Biology Through In Vivo Tracer Kinetics.Arteriosclerosis, thrombosis, and vascular biology · 2024
    Review
  15. Article
  16. HDL Function across the Lifespan: From Childhood, to Pregnancy, to Old Age.International journal of molecular sciences · 2023
    Review
  17. Article
  18. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 3 institutions in 1 country.

John T MelchiorDepartment of Pathology and Laboratory Medicine, Center for Lipid and Arteriosclerosis Science, University of Cincinnati, Cincinnati, OH 45237.
Scott E StreetDepartment of Pathology and Laboratory Medicine, Center for Lipid and Arteriosclerosis Science, University of Cincinnati, Cincinnati, OH 45237.
Allison B AndraskiDepartment of Nutrition, Harvard T. H. Chan School of Public Health, Boston, MA 02115.
Jeremy D FurtadoDepartment of Nutrition, Harvard T. H. Chan School of Public Health, Boston, MA 02115.
Frank M SacksDepartment of Nutrition, Harvard T. H. Chan School of Public Health, Boston, MA 02115; Department of Genetics & Complex Diseases, Harvard T. H. Chan School of Public Health, Boston, MA 02115.
Rebecca L ShuteDepartment of Pathology and Laboratory Medicine, Center for Lipid and Arteriosclerosis Science, University of Cincinnati, Cincinnati, OH 45237.
Emily I GreveDepartment of Pathology and Laboratory Medicine, Center for Lipid and Arteriosclerosis Science, University of Cincinnati, Cincinnati, OH 45237.
Debi K SwertfegerDivision of Biomedical Informatics Cincinnati Children's Hospital Research Foundation, Cincinnati, OH 45229.
Hailong LiDivision of Biomedical Informatics Cincinnati Children's Hospital Research Foundation, Cincinnati, OH 45229.
Amy S ShahDivision of Endocrinology, Department of Pediatrics, Cincinnati Children's Hospital Research Foundation, Cincinnati, OH 45229.
L Jason LuDivision of Biomedical Informatics Cincinnati Children's Hospital Research Foundation, Cincinnati, OH 45229.
W Sean DavidsonDepartment of Pathology and Laboratory Medicine, Center for Lipid and Arteriosclerosis Science, University of Cincinnati, Cincinnati, OH 45237. Electronic address: Sean.Davidson@UC.edu.
University of Cincinnati · USCincinnati Children's Hospital Medical Center · USHarvard University · US

Funding

Project 3 - HDL Structure/Function in LCAT Deficient HumansP01HL128203 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Tomas Vaisar · 2016 to 2026
$25.1M
Apolipoprotein A-I structure in high density lipoproteinsR01HL067093 · NHLBI · UNIVERSITY OF CINCINNATI · PI DAVIDSON, W SEAN · 2002 to 2016
$4.3M
A Network-based Approach to Associate HDL Subspeciation with FunctionR01HL111829 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI LU, LONG · 2012 to 2016
$2.6M
A high-resolution structural approach to understanding HDL biogenesisR01GM098458 · NIGMS · UNIVERSITY OF CINCINNATI · PI DAVIDSON, W SEAN · 2011 to 2014
$1.2M
Understanding the Role of HDL Subspecies in Adolescents with Type 2 DiabetesK23HL118132 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI SHAH, AMY SANGHAVI · 2014 to 2018
$855k
Enhanced proteomics capabilities for quantitation of proteins with a triple quadS10RR027015 · NCRR · UNIVERSITY OF CINCINNATI · PI GREIS, KENNETH DONALD · 2010 to 2010
$426k
NCRR NIH HHS S10 RR027015NHLBI NIH HHS K23 HL118132NHLBI NIH HHS P01 HL128203NHLBI NIH HHS R01 HL067093NHLBI NIH HHS R01 HL111829NIGMS NIH HHS R01 GM098458
6 · The paper itself

Abstract

HDLs are a family of heterogeneous particles that vary in size, composition, and function. The structure of most HDLs is maintained by two scaffold proteins, apoA-I and apoA-II, but up to 95 other "accessory" proteins have been found associated with the particles. Recent evidence suggests that these accessory proteins are distributed across various subspecies and drive specific biological functions. Unfortunately, our understanding of the molecular composition of such subspecies is limited. To begin to address this issue, we separated human plasma and HDL isolated by ultracentrifugation (UC-HDL) into particles with apoA-I and no apoA-II (LpA-I) and those with both apoA-I and apoA-II (LpA-I/A-II). MS studies revealed distinct differences between the subfractions. LpA-I exhibited significantly more protein diversity than LpA-I/A-II when isolated directly from plasma. However, this difference was lost in UC-HDL. Most LpA-I/A-II accessory proteins were associated with lipid transport pathways, whereas those in LpA-I were associated with inflammatory response, hemostasis, immune response, metal ion binding, and protease inhibition. We found that the presence of apoA-II enhanced ABCA1-mediated efflux compared with LpA-I particles. This effect was independent of the accessory protein signature suggesting that apoA-II induces a structural change in apoA-I in HDLs.

Indexed as

Apolipoprotein A-IApolipoprotein A-IIATP Binding Cassette Transporter 1Biological TransportHumansProteomeApolipoprotein A-IApolipoprotein A-IIATP Binding Cassette Transporter 1ProteomeATP binding cassette transporter A1high density lipoprotein/structureproteomics

Identifiers

PMID28476857
PMCPMC5496035
OpenAlexW2611915979

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.