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THE CONTRIBUTION OF ARACHIDONATE 5-LIPOXYGENASE TO INFLAMMATORY RESPONSE IN CORONARY ARTERY DISEASE
by
Susanna Vikman
A Thesis Presented to the
FACULTY OF THE USC GRADUATE SCHOOL
UNIVERSITY OF SOUTHERN CALIFORNIA
In Partial Fulfillment of the
Requirements for the Degree
MASTER OF SCIENCE
(BIOCHEMISTRY AND MOLECULAR BIOLOGY)
December 2010
Copyright 2010 Susanna Vikman
Object Description
| Title | The contribution of arachidonate 5-lipoxygenase to inflammatory response in coronary artery disease |
| Author | Vikman, Susanna |
| Author email | vikman@usc.edu; djsuzie@hotmail.com |
| Degree | Master of Science |
| Document type | Thesis |
| Degree program | Biochemistry & Molecular Biology |
| School | Keck School of Medicine |
| Date submitted | 2010 |
| Restricted until | Unrestricted |
| Date published | 2010-12-08 |
| Advisor (committee chair) | Tokes, Zoltan A. |
| Advisor (committee member) |
Joseph, Hacia Allayee, Hooman |
| Abstract | This study provides a review of the literature on coronary artery disease (CAD) focusing on the role of the enzyme 5-lipoxygenase (encoded by ALOX5) and in the regulatory pathways of ALOX5 in different human leukocyte populations. CAD affects millions of people being the leading cause of death in the world. Disease states contributing to CAD such as atherosclerosis present a highly complex and multi-factorial pathophysiology. Inflammation is recognized as being an important component in the development of CAD. Leukotrienes are potent inflammatory mediators produced from arachidonic acid through oxidative reaction catalyzed by 5-lipoxygenase (5-LO). Several reports have shown that leukotrienes are involved in the etiology of CAD. ALOX5 promoter polymorphism increased carotid artery intima-media thickness and that increased dietary arachidonic acid intake significantly enhanced the genotype effect. It is becoming apparent that hexanucleotide repeat variants of the ALOX5 promoter are differentially methylated and partly regulate ALOX5 expression in human lymphocytes. Homozygous shorter repeat variant showed higher gene expression than the homozygous wild type allele carriers in lymphocytes. Since atherosclerosis has an inflammatory component, it is important to better understand the role of immune response in the development of the disease. A recent study suggests the possibility of differential mechanism regulating ALOX5 expression in different human leukocyte populations. A new hypothesis concerning CAD is also discussed in this study. The recognition of the major risk factors contributing to CAD and improvements in therapies are critically important. |
| Keyword | 5-lipoxygenase; coronary artery disease; arachidonic acid metabolism; leukotriene; atherosclerosis |
| Language | English |
| Part of collection | University of Southern California dissertations and theses |
| Publisher (of the original version) | University of Southern California |
| Place of publication (of the original version) | Los Angeles, California |
| Publisher (of the digital version) | University of Southern California. Libraries |
| Provenance | Electronically uploaded by the author |
| Type | texts |
| Legacy record ID | usctheses-m3588 |
| Rights | Vikman, Susanna |
| Repository name | Libraries, University of Southern California |
| Repository address | Los Angeles, California |
| Repository email | http://www.usc.edu/isd/libraries/services/ask_a_librarian/email/ |
| Filename | etd-Vikman-4198 |
| Archival file | uscthesesreloadpub_Volume14/etd-Vikman-4198.pdf |
Description
| Title | Page 1 |
| Full text | THE CONTRIBUTION OF ARACHIDONATE 5-LIPOXYGENASE TO INFLAMMATORY RESPONSE IN CORONARY ARTERY DISEASE by Susanna Vikman A Thesis Presented to the FACULTY OF THE USC GRADUATE SCHOOL UNIVERSITY OF SOUTHERN CALIFORNIA In Partial Fulfillment of the Requirements for the Degree MASTER OF SCIENCE (BIOCHEMISTRY AND MOLECULAR BIOLOGY) December 2010 Copyright 2010 Susanna Vikman |
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