Evidence map›Paper›PMID 21030022›Full record

ArticleAtherosclerosis2010

Two adjacent domains (141-150 and 151-160) of apoE covalently linked to a class A amphipathic helical peptide exhibit opposite atherogenic effects.

Gaurav Nayyar, Shaila P Handattu, Candyce E Monroe, Manjula Chaddha, Geeta Datta, Vinod K Mishra, Tamara D Keenum, Mayakonda N Palgunachari, David W Garber, G M Anantharamaiah

Open access · greenAbstract read
In one paragraph

Article in Atherosclerosis, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

11 citing papers in PubMed, 25 citations in OpenAlex.

  1. Peptides as Therapeutic Agents for Atherosclerosis.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. A novel hemoglobin-binding peptide reduces cell-free hemoglobin in murine hemolytic anemia.American journal of physiology. Heart and circulatory physiology · 2013
    Article
  8. Article
  9. Article
  10. Article
  11. 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

10 authors at 1 institution in 1 country.

Gaurav NayyarAtherosclerosis Research Unit and Department of Medicine, Biochemistry and Molecular Genetics, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Shaila P Handattu
Candyce E Monroe
Manjula Chaddha
Geeta Datta
Vinod K Mishra
Tamara D Keenum
Mayakonda N Palgunachari
David W Garber
G M Anantharamaiah
University of Alabama at Birmingham · US

Funding

SYNTHETIC PEPTIDE STUDIES OF THE AMPHIPATHIC HELIXP01HL034343 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SEGREST, JERE P · 1985 to 2012
$18.8M
HDL Modulation of monocyte function in endotoxemiaR01GM082952 · NIGMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI DATTA, GEETA, WHITE, C ROGER · 2008 to 2011
$1.3M
NHLBI NIH HHS P01 HL034343NHLBI NIH HHS P01 HL34343NHLBI NIH HHS R01 HL0908030NIGMS NIH HHS R01 GM082952
6 · The paper itself

Abstract

objectiveWe recently described anti-atherogenic properties of the dual domain peptide Ac-hE18A-NH(2) derived by covalently linking the heparin binding domain 141-150 of apoE to 18A, a class A amphipathic helical peptide. In this paper we have compared the properties of Ac-hE18A-NH(2) with the non-heparin binding 151-160 region of apoE linked to 18A (Ac-nhE18A-NH(2)). METHODS AND

resultsBoth peptides were highly helical in solution and in association with lipids. Ac-hE18A-NH(2) and not Ac-nhE18A-NH(2) enhanced uptake of low density lipoprotein (LDL) in HepG2 cells. While Ac-hE18A-NH(2) retarded the electrophoretic mobility of LDL, Ac-nhE18A-NH(2) slightly enhanced mobility. Ac-hE18A-NH(2) reduced monocyte association with endothelial cells, while Ac-nhE18A-NH(2) increased it. Ac-hE18A-NH(2) also reduced lipid hydroperoxide content of LDL while Ac-nhE18A-NH(2) increased it. A single administration of Ac-hE18A-NH(2) (100 μg/mouse) into apoE null mice dramatically reduced cholesterol (from 600 mg/dL to 180 mg/dL at 5 min and to 60 mg/dL at 5h) while Ac-nhE18A-NH(2) had no effect. Administration (100 μg/mouse/day, three days a week) into apoE null mice for six weeks showed Ac-hE18A-NH(2) group having a moderate aortic sinus lesion reduction compared with the control group (-15.1%), while the Ac-nhE18A-NH(2) administered group had increased lesion area (+33.0% vs controls and 36.1% vs Ac-hE18A-NH(2)). Plasma from mice administered Ac-hE18A-NH(2) for six weeks showed a significant reduction in plasma cholesterol and triglyceride levels and increase in paraoxonase-1 (PON-1) activity compared to controls, while Ac-nhE18A-NH(2) caused no change in plasma cholesterol and decreased PON-1 activity.

conclusionIt is proposed that Ac-hE18A-NH(2) reduced lesion progression in apoE null mice due to its anti-inflammatory and lipoprotein clearing properties, while Ac-nhE18A-NH(2) exhibited pro-atherogenic effects.

Indexed as

AnimalsApolipoproteins EAryldialkylphosphataseAtherosclerosisCholesterolEndothelial CellsFemaleHeparan Sulfate ProteoglycansHep G2 CellsHumansLipoproteinsLipoproteins, LDLMiceMonocytesPeptide FragmentsProtein Structure, SecondaryAc-hE18A-NH(2)Apolipoproteins EAryldialkylphosphataseCholesterolHeparan Sulfate ProteoglycansLipoproteinsLipoproteins, LDLPeptide FragmentsTriglycerides

Identifiers

PMID21030022
PMCPMC2997865
OpenAlexW2024219510

What OpenQuestion holds

Textmetadata
LicenceTDM
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.