Evidence map›Paper›PMID 18366184›Full record

ArticleBiochemistry2008

The interplay between size, morphology, stability, and functionality of high-density lipoprotein subclasses.

Giorgio Cavigiolio, Baohai Shao, Ethan G Geier, Gang Ren, Jay W Heinecke, Michael N Oda

Open access · greenAbstract read
In one paragraph

Article in Biochemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
9.2field-weighted citation impact, top 2% 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

52 citing papers in PubMed, 94 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. High-Density Lipoproteins as Homeostatic Nanoparticles of Blood Plasma.International journal of molecular sciences · 2020
    Review
  7. Article
  8. Article
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  10. Article
  11. Article
  12. Article
  13. Article
  14. Methionine oxidized apolipoprotein A-I at the crossroads of HDL biogenesis and amyloid formation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    Article
  15. Tertiary structure of apolipoprotein A-I in nascent high-density lipoproteins.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  16. Assessing the mechanisms of cholesteryl ester transfer protein inhibitors.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2017
    Article
  17. Article
  18. Review
  19. Article
  20. Article
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

6 authors at 2 institutions in 1 country.

Giorgio CavigiolioChildren's Hospital Oakland Research Institute, Oakland, CA 94609, USA.
Baohai Shao
Ethan G Geier
Gang Ren
Jay W Heinecke
Michael N Oda
University of Washington · USUniversity of California, San Francisco · US

Funding

Serum Amyloid and Inflammation in AtherogenesisP01HL030086 · NHLBI · UNIVERSITY OF WASHINGTON · PI HEINECKE, JAY W · 1985 to 2009
$14.7M
Structure of apolipoprotein A-I on defined states of HDLR01HL077268 · NHLBI · CHILDREN'S HOSPITAL &RES CTR AT OAKLAND · PI ODA, MICHAEL NOBUAKI · 2004 to 2010
$2.0M
Molecular Mechanisms for Dysfunctional High Density Lipoprotein (HDL)R01HL086798 · NHLBI · UNIVERSITY OF WASHINGTON · PI HEINECKE, JAY W · 2007 to 2011
$1.9M
NHLBI NIH HHS HL 086708NHLBI NIH HHS HL 086798NHLBI NIH HHS HL 77268NHLBI NIH HHS P01 HL030086NHLBI NIH HHS R01 HL077268NHLBI NIH HHS R01 HL086798
6 · The paper itself

Abstract

High-density lipoprotein (HDL) mediates reverse cholesterol transport (RCT), wherein excess cholesterol is conveyed from peripheral tissues to the liver and steroidogenic organs. During this process HDL continually transitions between subclass sizes, each with unique biological activities. For instance, RCT is initiated by the interaction of lipid-free/lipid-poor apolipoprotein A-I (apoA-I) with ABCA1, a membrane-associated lipid transporter, to form nascent HDL. Because nearly all circulating apoA-I is lipid-bound, the source of lipid-free/lipid-poor apoA-I is unclear. Lecithin:cholesterol acyltransferase (LCAT) then drives the conversion of nascent HDL to spherical HDL by catalyzing cholesterol esterification, an essential step in RCT. To investigate the relationship between HDL particle size and events critical to RCT such as LCAT activation and lipid-free apoA-I production for ABCA1 interaction, we reconstituted five subclasses of HDL particles (rHDL of 7.8, 8.4, 9.6, 12.2, and 17.0 nm in diameter, respectively) using various molar ratios of 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine, free cholesterol, and apoA-I. Kinetic analyses of this comprehensive array of rHDL particles suggest that apoA-I stoichiometry in rHDL is a critical factor governing LCAT activation. Electron microscopy revealed specific morphological differences in the HDL subclasses that may affect functionality. Furthermore, stability measurements demonstrated that the previously uncharacterized 8.4 nm rHDL particles rapidly convert to 7.8 nm particles, concomitant with the dissociation of lipid-free/lipid-poor apoA-I. Thus, lipid-free/lipid-poor apoA-I generated by the remodeling of HDL may be an essential intermediate in RCT and HDL's in vivo maturation.

Indexed as

Apolipoprotein A-IHumansLipoproteins, HDLMicroscopy, ElectronParticle SizePhosphatidylcholine-Sterol O-AcyltransferaseRecombinant ProteinsApolipoprotein A-ILipoproteins, HDLPhosphatidylcholine-Sterol O-AcyltransferaseRecombinant Proteins

Identifiers

PMID18366184
PMCPMC2902722
OpenAlexW2028612087

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.