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Cardiovascular Research Advance Access originally published online on November 12, 2008
Cardiovascular Research 2009 81(1):3-4; doi:10.1093/cvr/cvn306
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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

Prokineticins and the heart: diverging actions elicited by signalling through prokineticin receptor-1 or -2

Håvard Attramadal1,2,3,*

1 Institute for Surgical Research, Rikshospitalet University Hospital, A3.1013, Sognsvannsveien, Oslo N-0027, Norway
2 Department of Cardiology, Rikshospitalet University Hospital, N-0027 Oslo, Norway
3 Center for Heart Failure Research, University of Oslo, N-0027 Oslo, Norway

* Corresponding author. Tel: +47 23073520; fax: 47 23073530. E-mail address: havard.attramadal@medisin.uio.no

This editorial refers to ‘Transgenic myocardial overexpression of prokineticin receptor-2 (GPR73b) induces hypertrophy and capillary leakage’ by K. Urayama et al.,4 pp. 28–37, this issue.

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

Prokineticins are a family of secreted, small, chemokine-like peptides first identified during the previous decade (for review see ref. 1 and 2). Two distinct members are currently known, prokineticin-1 and prokineticin-2, which mediate their biological activities by signalling through two homologous G protein-coupled receptors (7-transmembrane segment receptors), prokineticin receptor-1 (PKR-1), and prokineticin receptor-2 (PKR-2).1 Phylogenetically, the prokineticins display the highest similarity with defencins. Although our knowledge about the biological actions and pathophysiological implications of prokineticin-1 and -2 is in its infancy, current . . . [Full Text of this Article]


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Transgenic myocardial overexpression of prokineticin receptor-2 (GPR73b) induces hypertrophy and capillary vessel leakage
Kyoji Urayama, Deniz B. Dedeoglu, Célia Guilini, Stefan Frantz, Georg Ertl, Nadia Messaddeq, and Canan G. Nebigil
Cardiovasc Res 2009 81: 28-37. [Abstract] [Full Text] [PDF]