Evidence map›Paper›PMID 17580963›Full record

ArticleBiochemistry2007

Modification by acrolein, a component of tobacco smoke and age-related oxidative stress, mediates functional impairment of human apolipoprotein E.

Shiori Tamamizu-Kato, Jason Yiu Wong, Vikram Jairam, Koji Uchida, Vincent Raussens, Hiroyuki Kato, Jean-Marie Ruysschaert, Vasanthy Narayanaswami

Open access · greenAbstract read
In one paragraph

Article in Biochemistry, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

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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

8 authors at 3 institutions in 3 countries.

Shiori Tamamizu-KatoCenter for the Prevention of Obesity, Cardiovascular Disease and Diabetes, Children's Hospital Oakland Research Institute, 5700 Martin Luther King Jr. Way, Oakland, California 94609, USA.
Jason Yiu Wong
Vikram Jairam
Koji Uchida
Vincent Raussens
Hiroyuki Kato
Jean-Marie Ruysschaert
Vasanthy Narayanaswami
Nagoya University · JPUniversité Libre de Bruxelles · BEOakland University · US

Funding

SICKLE CELL SCHOLAR PLANU54HL070583 · NHLBI · CHILDREN'S HOSPITAL &RES CTR AT OAKLAND · PI VICHINKSY, ELLIOTT P. · 2003 to 2010
$12.0M
NCMHD Center of Excellence in Nutritional GenomicsP60MD000222 · NIMHD · UNIVERSITY OF CALIFORNIA DAVIS · PI RODRIGUEZ, RAYMOND L · 2003 to 2009
$8.4M
NHLBI NIH HHS U54 HL070583NIMHD NIH HHS P60 MD000222
6 · The paper itself

Abstract

Oxidative damage to proteins such as apolipoprotein B-100 increases the atherogenicity of low-density lipoproteins (LDL). However, little is known about the potential oxidative damage to apolipoprotein E (apoE), an exchangeable antiatherogenic apolipoprotein. ApoE plays an integral role in lipoprotein metabolism by regulating the plasma cholesterol and triglyceride levels. Hepatic uptake of lipoproteins is facilitated by apoE's ability to bind with cell surface heparan sulfate proteoglycans and to lipoprotein receptors via basic residues in its 22 kDa N-terminal domain (NT). We investigated the effect of acrolein, an aldehydic product of endogenous lipid peroxidation and a tobacco smoke component, on the conformation and function of recombinant human apoE3-NT. Acrolein caused oxidative modification of apoE3-NT as detected by Western blot with acrolein-lysine-specific antibodies, and tertiary conformational alterations. Acrolein modification impairs the ability of apoE3-NT to interact with heparin and the LDL receptor. Furthermore, acrolein-modified apoE3-NT displayed a 5-fold decrease in its ability to interact with lipid surfaces. Our data indicate that acrolein disrupts the functional integrity of apoE3, which likely interferes with its role in regulating plasma cholesterol homeostasis. These observations have implications regarding the role of apoE in the pathogenesis of smoking- and oxidative stress-mediated cardiovascular and cerebrovascular diseases.

Indexed as

AcroleinAgingApolipoprotein E3HeparinHumansOxidative StressPhospholipidsProtein Structure, TertiaryReceptors, LDLSmokingAcroleinApolipoprotein E3HeparinPhospholipidsReceptors, LDL

Identifiers

PMID17580963
PMCPMC2556514
OpenAlexW2064992681

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.