Modulation of atherogenesis by dietary gamma-linolenic acid

Y. Y. Fan, Kenneth Ramos, R. S. Chapkin

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Data from our in vitro studies indicate that macrophages isolated from mice fed GLA-enriched diets inhibit vascular SMC proliferation via a PGE1-cAMP dependent mechanism. Since SMC proliferation is one of the main events implicated in the pathogenesis of atherosclerosis (Ross, 1993), this anti-proliferative effect observed by dietary GLA is noteworthy. In vivo studies have established that dietary. GLA is capable of retarding the atherosclerotic lesion formation in ApoE knock out mice, an animal model that develops atherosclerosis similar to humans (Reddick, 1994). We propose that dietary GLA has the potential to inhibit SMC proliferation leading to retardation of atherosclerotic lesion formation, and therefore favorable modulation of the atherogenic process.

Original languageEnglish (US)
Pages (from-to)485-491
Number of pages7
JournalAdvances in Experimental Medicine and Biology
Volume469
StatePublished - 2000
Externally publishedYes

Fingerprint

gamma-Linolenic Acid
Macrophages
Alprostadil
Apolipoproteins E
Nutrition
Atherosclerosis
Animals
Modulation
Knockout Mice
Blood Vessels
Animal Models
Diet
In Vitro Techniques

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Modulation of atherogenesis by dietary gamma-linolenic acid. / Fan, Y. Y.; Ramos, Kenneth; Chapkin, R. S.

In: Advances in Experimental Medicine and Biology, Vol. 469, 2000, p. 485-491.

Research output: Contribution to journalArticle

@article{e3e6c2c96a994abbbcc9c29424d17253,
title = "Modulation of atherogenesis by dietary gamma-linolenic acid",
abstract = "Data from our in vitro studies indicate that macrophages isolated from mice fed GLA-enriched diets inhibit vascular SMC proliferation via a PGE1-cAMP dependent mechanism. Since SMC proliferation is one of the main events implicated in the pathogenesis of atherosclerosis (Ross, 1993), this anti-proliferative effect observed by dietary GLA is noteworthy. In vivo studies have established that dietary. GLA is capable of retarding the atherosclerotic lesion formation in ApoE knock out mice, an animal model that develops atherosclerosis similar to humans (Reddick, 1994). We propose that dietary GLA has the potential to inhibit SMC proliferation leading to retardation of atherosclerotic lesion formation, and therefore favorable modulation of the atherogenic process.",
author = "Fan, {Y. Y.} and Kenneth Ramos and Chapkin, {R. S.}",
year = "2000",
language = "English (US)",
volume = "469",
pages = "485--491",
journal = "Advances in Experimental Medicine and Biology",
issn = "0065-2598",
publisher = "Springer New York",

}

TY - JOUR

T1 - Modulation of atherogenesis by dietary gamma-linolenic acid

AU - Fan, Y. Y.

AU - Ramos, Kenneth

AU - Chapkin, R. S.

PY - 2000

Y1 - 2000

N2 - Data from our in vitro studies indicate that macrophages isolated from mice fed GLA-enriched diets inhibit vascular SMC proliferation via a PGE1-cAMP dependent mechanism. Since SMC proliferation is one of the main events implicated in the pathogenesis of atherosclerosis (Ross, 1993), this anti-proliferative effect observed by dietary GLA is noteworthy. In vivo studies have established that dietary. GLA is capable of retarding the atherosclerotic lesion formation in ApoE knock out mice, an animal model that develops atherosclerosis similar to humans (Reddick, 1994). We propose that dietary GLA has the potential to inhibit SMC proliferation leading to retardation of atherosclerotic lesion formation, and therefore favorable modulation of the atherogenic process.

AB - Data from our in vitro studies indicate that macrophages isolated from mice fed GLA-enriched diets inhibit vascular SMC proliferation via a PGE1-cAMP dependent mechanism. Since SMC proliferation is one of the main events implicated in the pathogenesis of atherosclerosis (Ross, 1993), this anti-proliferative effect observed by dietary GLA is noteworthy. In vivo studies have established that dietary. GLA is capable of retarding the atherosclerotic lesion formation in ApoE knock out mice, an animal model that develops atherosclerosis similar to humans (Reddick, 1994). We propose that dietary GLA has the potential to inhibit SMC proliferation leading to retardation of atherosclerotic lesion formation, and therefore favorable modulation of the atherogenic process.

UR - http://www.scopus.com/inward/record.url?scp=0034465485&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034465485&partnerID=8YFLogxK

M3 - Article

C2 - 10667372

AN - SCOPUS:0034465485

VL - 469

SP - 485

EP - 491

JO - Advances in Experimental Medicine and Biology

JF - Advances in Experimental Medicine and Biology

SN - 0065-2598

ER -