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Cardiovascular Research Advance Access [Accepted Manuscript] published online on August 14, 2008
Cardiovascular Research, doi:10.1093/cvr/cvn227
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

Atherosclerosis development in apolipoprotein E-null mice deficient for CD69

Manuel Gómez1,5, Silvia M. Sanz-González2,4,5, Yafa Naim Abu Nabah2, Amalia Lamana1, Francisco Sánchez-Madrid1,3 and Vicente Andrés2,6

1 Servicio de Inmunología, Hospital de la Princesa, Universidad Autónoma de Madrid, Madrid, Spain
2 Laboratory of Vascular Biology, Department of Molecular and Cellular Pathology and Therapy, Instituto de Biomedicina de Valencia, Consejo Superior de Investigaciones Científicas, Valencia, Spain
3 Departamento de Biología Vascular e Inflamación. Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain

6 To whom correspondence should be addressed: Vicente Andrés, PhD, Instituto de Biomedicina de Valencia., C/ Jaime Roig 11, 46010. Valencia ( Spain), Phone: +34 963391752Fax: +34 963391751 E-mail: vandres{at}ibv.csic.es

AIMS: Atherosclerosis is a chronic inflammatory disease regulated by immune mechanisms. CD69 is a cell surface receptor rapidly induced after leukocyte activation at sites of chronic inflammation. Genetic disruption of CD69 in the mouse aggravates collagen-induced arthritis (CIA), and partial depletion of CD69 expressing cells with anti-CD69 monoclonal antibody (mAb) prevents CIA development in wild-type mice, suggesting that this receptor negatively modulates immune and inflammatory responses. It has been recently reported that CD69 is upregulated in a large subset of T cells in atherosclerosis-prone apolipoprotein E-null mice (apoE-/-). In this study, we investigated whether altering CD69 function affects atherosclerosis development.

METHODS: We studied native and diet-induced atherosclerosis in apoE-/- and doubly deficient apoE-/-CD69-/- mice and performed expression studies in tissues and primary cells derived from these animals.

RESULTS: Plasma cholesterol level was unaffected by CD69 genetic inactivation. Whilst this genetic manipulation led to an elevated production of interferon {gamma} and interleukin 10 by activated T cells, apoE-/- and apoE-/-CD69-/- mice fed control and high-fat diet exhibited atheromas of similar size and composition when analyzed at different stages of the disease. Likewise, anti-CD69 mAb treatment had no effect on plasma cholesterol and atherosclerosis burden in fat-fed apoE-/- mice.

CONCLUSIONS: In contrast to previous studies highlighting the protective function of CD69 against CIA, an autoimmune inflammatory disease, our results rule out a significant role for CD69 against atherosclerosis in apoE-/- mice, an experimental disease model featuring a local inflammatory response triggered and sustained by alterations in lipid homeostasis.

Time for primary review: 20 Days

4 Present address: Centro de Investigación Príncipe Felipe, Valencia, Spain.

5 Authors with equal contribution


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