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Stress, inflammation, and atheroscle...

Georgetown University Medical Center.

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Stress, inflammation, and atherosclerosis.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Stress, inflammation, and atherosclerosis./
Author:	Andrews, James A.
Description:	251 p.
Notes:	Advisers: Mary Susan Burnett; Zofia Zukowska.
Contained By:	Dissertation Abstracts International70-01B.
Subject:	Biology, Animal Physiology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3345522
ISBN:	9781109005615

Stress, inflammation, and atherosclerosis.
Andrews, James A.

Stress, inflammation, and atherosclerosis. - 251 p.

Advisers: Mary Susan Burnett; Zofia Zukowska.

Thesis (Ph.D.)--Georgetown University Medical Center, 2008.

Atherosclerosis is a pervasive disease. We hypothesized that chronic stress, such as chronic cold stress, and murine cytomegalovirus (MCMV) infection exacerbate inflammation and atherosclerosis. Neuropeptide-Y (NPY), a sympathetic co-transmitter, may mediate the effects of chronic stress on atherosclerosis. We investigated the effects of chronic stress and MCMV infection on cytokines, mediators of inflammation. Hyperlipidemic apolipoprotein-E knockout (ApoE KO) mice were utilized in studies of atherosclerotic lesion development.

ISBN: 9781109005615Subjects--Topical Terms:

1017835
Biology, Animal Physiology.

Stress, inflammation, and atherosclerosis.
LDR:03433nam 2200313 a 45 001 855257
005 20100708
008 100708s2008 ||||||||||||||||| ||eng d
020 $a 9781109005615
035 $a (UMI)AAI3345522
035 $a AAI3345522
040 $a UMI $c UMI
100 1 $a Andrews, James A. $3 1021822
245 1 0 $a Stress, inflammation, and atherosclerosis.
300 $a 251 p.
500 $a Advisers: Mary Susan Burnett; Zofia Zukowska.
500 $a Source: Dissertation Abstracts International, Volume: 70-01, Section: B, page: 0022.
502 $a Thesis (Ph.D.)--Georgetown University Medical Center, 2008.
520 $a Atherosclerosis is a pervasive disease. We hypothesized that chronic stress, such as chronic cold stress, and murine cytomegalovirus (MCMV) infection exacerbate inflammation and atherosclerosis. Neuropeptide-Y (NPY), a sympathetic co-transmitter, may mediate the effects of chronic stress on atherosclerosis. We investigated the effects of chronic stress and MCMV infection on cytokines, mediators of inflammation. Hyperlipidemic apolipoprotein-E knockout (ApoE KO) mice were utilized in studies of atherosclerotic lesion development.
520 $a Chronic cold stress (CS) involved placing mice (WT or ApoEKO) in shallow ice water 1 h daily for 28 consecutive days. Serum NPY, corticosterone (only in ApoEKO), and cytokines (IL-1beta, IFN-gamma, TNF-alpha, IL-10, IL-6, MCP-1, and resistin) were measured two hours and one day after the final cold stress exposure. In ApoEKO mice exposed to chronic cold stress or MCMV infection, atherosclerotic lesion development was evaluated.
520 $a Chronically stressed ApoEKO mice demonstrated more advanced atherosclerotic lesions, as well as increased serum NPY, corticosterone, IL-1beta, IFN-gamma, TNF-alpha, IL-10, I and resistin levels, and decreased IL-6 levels, overall a pro-atherosclerotic cytokine profile, as compared to non-stressed ApoEKO mice. In contrast, a single cold stress exposure did not affect cytokine levels. Whereas, CS increased serum NPY in all mouse groups, wildtype mice (WT) fed either high-fat (WTHF) or normal chow (WTNC) had disparate stress-induced cytokine responses. High-fat intake appeared to enhance stress-induced cytokine responses. Moreover, the stress-induced increase in circulating resistin was temporally delayed; it was not evident two hours after CS exposure, but it appeared twenty-four hours later. Overall these findings support the association of CS with inflammation and strengthen the contention that CS accelerates atherosclerosis. MCMV-infected ApoEKO mice had elevated cytokine levels, and previous studies showed that MCMV infection enhances atherosclerotic lesion formation.
520 $a In summary, we conclude that chronic stress or MCMV infection may exacerbate atherosclerosis via increased inflammation. Levels of corticosteroids and lipids may amplify these effects. We propose that chronic stress may directly exacerbate inflammation within atheromata by release of NPY, and from a distance via circulating inflammatory mediators. More research is needed to establish causality between these various factors.
590 $a School code: 0544.
650 4 $a Biology, Animal Physiology. $3 1017835
690 $a 0433
710 2 $a Georgetown University Medical Center. $3 1021821
773 0 $t Dissertation Abstracts International $g 70-01B.
790 $a 0544
790 1 0 $a Burnett, Mary Susan, $e advisor
790 1 0 $a Zukowska, Zofia, $e advisor
791 $a Ph.D.
792 $a 2008
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3345522