PGE2-mediated podosome loss in dendritic cells is dependent on actomyosin contraction downstream of the RhoA-Rho-kinase axis.
Publication year
2008Source
Journal of Cell Science, 121, Pt 7, (2008), pp. 1096-1106ISSN
Publication type
Article / Letter to editor

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Organization
Tumorimmunology
Paediatrics
Journal title
Journal of Cell Science
Volume
vol. 121
Issue
iss. Pt 7
Page start
p. 1096
Page end
p. 1106
Subject
NCMLS 1: Immunity, infection and tissue repair; NCMLS 2: Immune Regulation; ONCOL 2: Age-related aspects of cancer; ONCOL 3: Translational research; UMCN 1.4: Immunotherapy, gene therapy and transplantationAbstract
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.
This item appears in the following Collection(s)
- Academic publications [204107]
- Faculty of Medical Sciences [80531]
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