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First published online 11 March 2008
doi: 10.1242/jcs.020289

Journal of Cell Science 121, 1096-1106 (2008)
Published by The Company of Biologists 2008
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Research Article

PGE2-mediated podosome loss in dendritic cells is dependent on actomyosin contraction downstream of the RhoA–Rho-kinase axis

Suzanne F. G. van Helden1, Machteld M. Oud1, Ben Joosten1, Niels Peterse2, Carl G. Figdor1,* and Frank N. van Leeuwen2

1 Department of Tumor Immunology, Nijmegen Centre for Molecular Life Sciences, Radboud University Nijmegen Medical Centre, PO Box 9101, 6500 HB Nijmegen, The Netherlands
2 Laboratory of Pediatric Oncology, Nijmegen Centre for Molecular Life Sciences, Radboud University Nijmegen Medical Centre, PO Box 9101, 6500 HB Nijmegen, The Netherlands

* Author for correspondence (e-mail: c.figdor{at}ncmls.ru.nl)

Accepted 16 January 2008

Podosomes are dynamic adhesion structures found in dendritic cells (DCs) and other cells of the myeloid lineage. We previously showed that prostaglandin E2 (PGE2), an important proinflammatory mediator produced during DC maturation, induces podosome disassembly within minutes after stimulation. Here, we demonstrate that this response is mediated by cAMP elevation, occurs downstream of Rho kinase and is dependent on myosin II. Whereas PGE2 stimulation leads to activation of the small GTPase RhoA, decreased levels of Rac1-GTP and Cdc42-GTP are observed. These results show that PGE2 stimulation leads to activation of the RhoA–Rho-kinase axis to promote actomyosin-based contraction and subsequent podosome dissolution. Because podosome disassembly is accompanied by de novo formation of focal adhesions, we propose that the disassembly/formation of these two different adhesion structures is oppositely regulated by actomyosin contractility and relative activities of RhoA, Rac1 and Cdc42.

Key words: Dendritic cell, PGE2, Podosomes, Actomyosin contraction, RhoA


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