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Cardiovascular Research Advance Access first published online on August 14, 2009
This version [Corrected Proof] published online on September 18, 2009
Cardiovascular Research, doi:10.1093/cvr/cvp278
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

Resistin: a newly identified chemokine for human CD4-positive lymphocytes

Daniel Walcher, Katharina Hess, Rebecca Berger, Milos Aleksic, Philipp Heinz, Helga Bach, Renate Durst, Angelina Hausauer, Vinzenz Hombach and Nikolaus Marx*

Department of Internal Medicine II—Cardiology, University of Ulm, Robert-Koch-Str. 8, D-89081 Ulm, Germany

* Corresponding author. Tel: +49 731 500 45000, Fax: +49 731 500 45025, Email: nikolaus.marx{at}medizin.uni-ulm.de

Aims: Increased levels of resistin, a peptide secreted by adipocytes and inflammatory cells, circulate in patients with insulin resistance and early type 2 diabetes, a high-risk population for the development of a diffuse and extensive pattern of arteriosclerosis. Recent data suggest that resistin may activate vascular cells such as smooth muscle cells and endothelial cells, but hitherto nothing is known about the role of resistin in CD4-positive lymphocytes. Therefore, the present study examined the effect of resistin on CD4-positive lymphocyte migration, an important process in early atherogenesis.

Methods and results: Resistin stimulated CD4-positive cell chemotaxis in a concentration-dependent manner with a maximal induction of 2.25 ± 0.54 at 100 ng/mL (P < 0.05, n = 7). This process involves pertussis toxin-sensitive G-proteins as well as activation of Src- and phosphoinositide 3-kinase (PI 3-K). Biochemical analysis showed that resistin induces phosphorylation of Src and PI 3-K activation in human CD4-positive cells. In addition, resistin activates RhoA, Rac-1, and Cdc42 in these cells as shown by affinity precipitation experiments. Finally, resistin-induced phosphorylation of myosin light chain was inhibited by Src short interference RNA transfection, underscoring the importance of the upstream signalling molecule Src in resistin-induced migration.

Conclusion: These data support an active role of resistin in CD4-positive lymphocyte chemotaxis and elucidate molecular mechanisms in resistin-induced cell migration.

KEYWORDS Resistin; CD4-positive lymphocytes; Migration; Signalling; Atherosclerosis

Time for primary review: 19 days


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