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Barlic-Dicen, Jana

Jana Barlic-Dicen, Ph.D.

Jana Barlic-Dicen, Ph.D.

Assistant Member
Cardiovascular Biology Research Program

Adjunct Assistant Professor, Department of Cell Biology University of Oklahoma Health Sciences Center

One of the most serious heart conditions affecting Americans today is heart disease resulting from atherosclerosis. This disorder occurs when blood vessel walls thicken because of the fatty deposits called plaques that can block blood flow and lead to the onset of heart or artery disease.

Atherosclerosis occurs when low-density lipoprotein (LDL), the so-called “bad” cholesterol, is processed inside the vessel walls and becomes oxidized. Because of the excess of oxidized LDL in the arterial wall, alarm signals are sent to the white blood cells, the body’s disease fighters, causing them to flood the affected vessel walls in an attempt to clean up the LDL. Instead, the white blood cells become trapped in plaques leading to more buildup, which leads to progressive heart disease. If a piece of the plaque breaks off, it can cause a heart attack or stroke.

In my lab, we study chemokines, the proteins in the body that sound the alarm to send the white blood cells into the affected vessel walls. Although chemokine production is associated with plaque growth and therefore atherosclerosis progression, we have learned that, in some cases, chemokines protect the vessels from atherosclerosis and may even stimulate plaques to regress.

We want to learn how chemokines oppose atherosclerosis and how they trigger the process of plaque regression to develop ways that the body can protect itself from atherosclerosis. Few people realize they have heart disease until damage occurs or until they fall victim to a heart attack or stroke, so many stand to benefit from approaches and treatments that will interfere with atherosclerosis or reverse plaque buildup. By using mouse models of atheroprotection and atheroregression, we can look for the mechanisms that interfere with atherosclerosis or lead to regression of this disease and find ways to stimulate it in people who already have it.

B.Sc. (honors), University of Ljubljana, Slovenia, 1995
Ph.D., University of Western Ontario, London, Ontario, Canada, 2001
Post-doctoral training, Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, 2007

Honors and Awards
Wellcome Trust Research Career Development Award in Basic Biomedical Science

American Association for the Advancement of Science
British Society for Immunology

Joined OMRF Scientific Staff in 2008.

Within 10 years, cardiovascular disease will be the major cause of mortality worldwide owing to its rapidly increasing prevalence in developing countries, Eastern Europe and the Western world. A process underlying cardiovascular disease, including coronary artery disease, heart failure and stroke, is atherosclerosis. It is hypothesized that hypertension, as well as accumulation and oxidation of low density lipoprotein in the intima, are major factors initiating atherosclerotic vascular inflammation, which is characterized by continuous and persistent recruitment of leukocytes into the vascular sub-endothelium.

Important promoters of leukocyte influx into the inflamed arterial wall are chemotactic cytokines (chemokines), which stimulate leukocyte recruitment into atherosclerotic lesions through interactions with chemokine receptors. In addition, it is thought that chemokines and chemokine receptors may also coordinate communication between inflammatory cellular components in peripheral blood and cellular components of the arterial wall, thereby regulating leukocyte capture that promotes atherosclerosis. In contrast to these two paradigms, chemokines were demonstrated to protect against atherosclerosis. However, mechanisms of chemokine-dependent atheroprotection have not been identified or characterized. Nevertheless, although it is currently thought that chemokines and their receptors facilitate the resolution of vascular inflammation by mobilizing the pathologic components of the plaque, we still do not understand why the process of plaque regression is severely impaired in atherosclerosis.

We will investigate chemokine-dependent mechanisms of atheroprotection and atheroregression, because we maintain that results of these studies will further our knowledge of the comprehensive contributions of chemokines in atherosclerosis and may suggest new opportunities for prevention of or therapy for this complex disease.

Recent Publications

Kwak JY, Mamura M, Barlic-Dicen J, Grage-Griebenow E. Pathophysiological roles of cytokine-chemokine immune network. J Immunol Res 2014;2014:615130. [Abstract]

* Yao L, Heuser-Baker J, Herlea-Pana O, Zhang N, Szweda LI, Griffin TM, Barlic-Dicen J. Deficiency in adipocyte chemokine receptor CXCR4 exacerbates obesity and compromises thermoregulatory responses of brown adipose tissue in a mouse model of diet-induced obesity. FASEB J 2014. [Abstract] EPub

Yao L, Herlea-Pana O, Heuser-Baker J, Chen Y, Barlic-Dicen J. Roles of the Chemokine System in Development of Obesity, Insulin Resistance, and Cardiovascular Disease. J Immunol Res 2014:181450, 2014. [Abstract]

Selected Publications
Barlic J, Zhang Y, Foley JF, Murphy PM. Oxidized lipid-driven chemokine receptor switch, CCR2 to CX3CR1, mediates adhesion of human macrophages to coronary artery smooth muscle cells through a peroxisome proliferator-activated receptor gamma-dependent pathway. Circulation 114:807-819, 2006. Abstract]

Barlic J, McDermott DH, Merrell MN, Gonzales J, Via LE, Murphy PM. Interleukin (IL-15) and IL-2 reciprocally regulate expression of the chemokine receptor CX3CR1 through selective NFAT1- and NFAT2-dependent mechanisms. J Biol Chem 279:48520-49534, 2004. [Abstract]

Barlic J, Sechler JM, Murphy PM. IL-15 and IL-2 oppositely regulate expression of the chemokine receptor CX3CR1. Blood 102:3494-3503, 2003. [Abstract]

Barlic J, Andrews JD, Kelvin AA, Bosinger SE, DeVries ME, Xu L, Dobransky T, Feldman RD, Ferguson SSG, Kelvin DJ. Regulation of tyrosine kinase activation and granule release through b-arrestin by CXCR1. Nat Immunol 1:227-233, 2000. [Abstract]

View all publications in PubMed

Cardiovascular Biology Research Program, MS 45
Oklahoma Medical Research Foundation
825 N.E. 13th Street
Oklahoma City, OK 73104

Phone: (405) 271-2560
Fax: (405) 271-3137

Longbiao Yao, M.D.
Staff Scientist

Oana-Miheala Herlea-Pana, Ph.D.
Assistant Staff Scientist

Janet Heuser-Baker
Senior Research Assistant

Mia Pederson-Rambo
Executive Assistant