Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 14-Day Trial for You or Your Team.

Learn More →

The CX 3

The CX 3 The CX C Chemokine Fractalkine Induces Vascular Dysfunction by Generation of Superoxide Anions Andreas Scha¨fer, Christian Schulz, Daniela Fraccarollo, Piet Tas, Meike Leutke, Martin Eigenthaler, Stefan Seidl, Peter Heider, Georg Ertl, Steffen Massberg, Johann Bauersachs Objective—The chemokine fractalkine activates platelets and induces leukocyte adhesion to the endothelium. Expression of fractalkine and its receptor, CX CR1, is elevated in coronary artery disease. We assessed the effects of fractalkine on vascular function in isolated rat aorta. Methods and Results—CX CR1 expression was demonstrated in rat aortic endothelial and smooth muscle cells by immunohistochemistry, Western blot, and polymerase chain reaction (PCR). Fractalkine (up to 1 g/mL) did not directly induce contractile or relaxant responses when applied to rat aortic rings in organ baths. Short-term incubation with fractalkine (1 g/mL) for 5 minutes did not affect vascular reactivity. Pretreatment of isolated rat aortic rings with fractalkine for 2 hours impaired acetylcholine-induced nitric oxide (NO)-mediated relaxation after preconstriction with phenylephrine in a concentration-dependent manner. The concentration response to the NO donor DEA-NONOate was significantly shifted to the right. The radical scavenger tiron normalized the attenuated acetylcholine-induced relaxation after fractalkine incubation. Aortic superoxide formation was enhanced by fractalkine, which was inhibited by diphenyleneiodonium but not http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Arteriosclerosis, Thrombosis, and Vascular Biology Wolters Kluwer Health

The CX 3

Download PDF
8 pages

Loading next page...
 
/lp/wolters-kluwer-health/the-cx-3-IJ0DqNLtxa

References

References for this paper are not available at this time. We will be adding them shortly, thank you for your patience.

ISSN
1079-5642
eISSN
1524-4636
DOI
10.1161/01.ATV.0000251535.30191.60
pmid
17082482
Publisher site
See Article on Publisher Site

Abstract

The CX C Chemokine Fractalkine Induces Vascular Dysfunction by Generation of Superoxide Anions Andreas Scha¨fer, Christian Schulz, Daniela Fraccarollo, Piet Tas, Meike Leutke, Martin Eigenthaler, Stefan Seidl, Peter Heider, Georg Ertl, Steffen Massberg, Johann Bauersachs Objective—The chemokine fractalkine activates platelets and induces leukocyte adhesion to the endothelium. Expression of fractalkine and its receptor, CX CR1, is elevated in coronary artery disease. We assessed the effects of fractalkine on vascular function in isolated rat aorta. Methods and Results—CX CR1 expression was demonstrated in rat aortic endothelial and smooth muscle cells by immunohistochemistry, Western blot, and polymerase chain reaction (PCR). Fractalkine (up to 1 g/mL) did not directly induce contractile or relaxant responses when applied to rat aortic rings in organ baths. Short-term incubation with fractalkine (1 g/mL) for 5 minutes did not affect vascular reactivity. Pretreatment of isolated rat aortic rings with fractalkine for 2 hours impaired acetylcholine-induced nitric oxide (NO)-mediated relaxation after preconstriction with phenylephrine in a concentration-dependent manner. The concentration response to the NO donor DEA-NONOate was significantly shifted to the right. The radical scavenger tiron normalized the attenuated acetylcholine-induced relaxation after fractalkine incubation. Aortic superoxide formation was enhanced by fractalkine, which was inhibited by diphenyleneiodonium but not

Journal

Arteriosclerosis, Thrombosis, and Vascular Biology – Wolters Kluwer Health

Published: Jan 1, 2007

There are no references for this article.