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

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

Research Abstract Table of Contents

Jump to the:

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

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

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.

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

S Tamamizu-Kato,JY Wong,V Jairam,K Uchida,V Raussens,H Kato,JM Ruysschaert,V Narayanaswami,

For similar behavior and behavior mechanisms: behavior: habits: smoking research abstracts see: behavior and behavior mechanisms: behavior: habits: smoking research

PUBMED ID PMID:

MEDLINE DATE:

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

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Biochemistry

VOLUME: 46

Page Numbers: 8392-400

Journal Abbreviation: Biochemistry

ISSN: 0006-2960

DAY: 20

MONTH: 06

YEAR: 2007

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

Number of References:

LANGUAGE: eng

NlmUniqueID: 370623

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

KEYWORDS: Smoking

MESH TERMS: metabolism

Chemical & Substance for Abstract: Modification by acrolein, a component of tobacco smoke and age-related oxidative stress, mediates functional impairment of human apolipoprotein E. Information

Substance Name: Heparin

Registry Number: 9005-49-6

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

AFFILIATION: Center 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.

Country: United States

AGENCY: United States NCMHD

GRANT: P60 MD000222

ACRONYM: MD

MEDLINETA: Biochemistry

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

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

• Interaction with amyloid Beta Peptide compromises the lipid binding function of apolipoprotein e.
• Modification by acrolein, a component of tobacco smoke and age-related oxidative stress, mediates functional impairment of human apolipoprotein E.