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Cardiovascular Research Advance Access originally published online on November 2, 2008
Cardiovascular Research 2009 81(1):9-10; doi:10.1093/cvr/cvn293
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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

Secretory phospholipase A2 type IIA: a regulator of immune function in atherosclerosis?

Alexander Bobik*

Vascular Biology and Atherosclerosis Laboratory, Baker Heart and Diabetes Institute, PO Box 6492, St Kilda Road Central, Melbourne, Vic 8008, Australia

* Corresponding author. Tel: +61 3 8532 1190; fax: 61 3 8532 1100. E-mail address: alex.bobik@bakeridi.edu.au

This editorial refers to ‘Secreted phospholipase A2 type IIA as a mediator connecting innate and adaptive immunity: new role in atherosclerosis’, by E. Ibeas et al.,4 pp. 54–63, this issue.

The first 10% of the full text of this article appears below.

Soluble phospholipase A2 type IIA (sPLA2-IIA) is an acute-phase reactant that is markedly increased in inflammatory disorders including cardiovascular disease. Inflammatory cytokines such as interleukins IL-6 and IL-1β, interferon (IFN)-{gamma}, and tumour necrosis factor (TNF)-{alpha} increase its expression in vascular smooth muscle cells and hepatocytes, two cell types largely responsible for its elevations in plasma. sPLA2-IIA is also highly expressed in atherosclerotic lesions and associated with smooth muscle cells, macrophages, and glycoaminoglycans,1 where it exerts proatherogenic effects in part by modifying low-and high-density lipoproteins (LDL and HDL). It hydrolyses the sn-2 . . . [Full Text of this Article]


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Secreted phospholipase A2 type IIA as a mediator connecting innate and adaptive immunity: new role in atherosclerosis
Elvira Ibeas, Lucía Fuentes, Rubén Martín, Marita Hernández, and Maria Luisa Nieto
Cardiovasc Res 2009 81: 54-63. [Abstract] [Full Text] [PDF]