|
|
|
|
|
||
|
|||||
| Home Help Feedback Subscriptions Archive Search Table of Contents | |||||
First published online May 24, 2006
doi: 10.1242/10.1242/jcs.02939
Research Article |
1 Randall Division of Cell and Molecular Biophysics, King's College London, New Hunt's House, Guy's Campus, London, SE1 1UL, UK
2 Advanced Science and Technology Laboratory, AztraZeneca Charnwood, Loughborough, LE11 5RH, UK
3 Molecular Immunology Unit, Institute of Child Health, University College London, WC1N 1EH, UK
* Authors for correspondence (e-mail: yolanda.calle{at}kcl.ac.uk; gareth.jones{at}kcl.ac.uk)
Accepted 15 February 2006
Podosomes, highly dynamic adhesion structures implicated in cell motility and extracellular matrix degradation, are characteristic of certain cells of the myeloid lineage and a limited range of other cell types. The nature and the mechanisms that regulate their high turnover are unknown at present. The cysteine protease calpain is involved in the regulation of cell migration in part by promoting either formation or disassembly of adhesion sites. Despite the fact that many known substrates of calpain are also structural components of the podosome complex, no studies have yet demonstrated that calpain participates in the regulation of podosome dynamics. In the present work, we show that inhibition of calpain in primary mouse dendritic cells leads to enhanced accumulation of actin filaments, the Wiskott Aldrich Syndrome protein (WASP), ß2 integrins, talin, paxillin and vinculin in podosomes. This accumulation of components is associated with stabilisation of podosome turnover, overall reduction in velocity of cell locomotion and impaired transmigration across an endothelial monolayer. We also demonstrate that calpain cleaves the podosome components talin, Pyk2 and WASP in dendritic cells. In summary, our results provide evidence that calpain regulates podosome composition and turnover and that this process is required for efficient migration of dendritic cells.
Key words: Cell motility, Leukocyte, Dendritic cell, Podosome, Cell adhesion, Calpain
This article has been cited by other articles:
|
|
 |
|
  H. Dinh, G. M. Scholz, and J. A. Hamilton Regulation of WAVE1 expression in macrophages at multiple levels J. Leukoc. Biol., December 1, 2008; 84(6): 1483 - 1491. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Obermajer, U. Svajger, M. Bogyo, M. Jeras, and J. Kos Maturation of dendritic cells depends on proteolytic cleavage by cathepsin X J. Leukoc. Biol., November 1, 2008; 84(5): 1306 - 1315. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. A. West, A. R. Prescott, K. M. Chan, Z. Zhou, S. Rose-John, J. Scheller, and C. Watts TLR ligand-induced podosome disassembly in dendritic cells is ADAM17 dependent J. Cell Biol., September 8, 2008; 182(5): 993 - 1005. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. F. G. van Helden, M. M. Oud, B. Joosten, N. Peterse, C. G. Figdor, and F. N. van Leeuwen PGE2-mediated podosome loss in dendritic cells is dependent on actomyosin contraction downstream of the RhoA-Rho-kinase axis J. Cell Sci., April 1, 2008; 121(7): 1096 - 1106. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. L. Cortesio, K. T. Chan, B. J. Perrin, N. O. Burton, S. Zhang, Z.-Y. Zhang, and A. Huttenlocher Calpain 2 and PTP1B function in a novel pathway with Src to regulate invadopodia dynamics and breast cancer cell invasion J. Cell Biol., March 5, 2008; 180(5): 957 - 971. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Badowski, G. Pawlak, A. Grichine, A. Chabadel, C. Oddou, P. Jurdic, M. Pfaff, C. Albiges-Rizo, and M. R. Block Paxillin Phosphorylation Controls Invadopodia/Podosomes Spatiotemporal Organization Mol. Biol. Cell, February 1, 2008; 19(2): 633 - 645. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Chabadel, I. Banon-Rodriguez, D. Cluet, B. B. Rudkin, B. Wehrle-Haller, E. Genot, P. Jurdic, I. M. Anton, and F. Saltel CD44 and beta3 Integrin Organize Two Functionally Distinct Actin-based Domains in Osteoclasts Mol. Biol. Cell, December 1, 2007; 18(12): 4899 - 4910. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Tsuboi and J. Meerloo Wiskott-Aldrich Syndrome Protein Is a Key Regulator of the Phagocytic Cup Formation in Macrophages J. Biol. Chem., November 23, 2007; 282(47): 34194 - 34203. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Kato, S. Khan, E. d'Aniello, K. J. McDonald, and D. N. J. Hart The Novel Endocytic and Phagocytic C-Type Lectin Receptor DCL-1/CD302 on Macrophages Is Colocalized with F-Actin, Suggesting a Role in Cell Adhesion and Migration J. Immunol., November 1, 2007; 179(9): 6052 - 6063. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. B. Yaroslavskiy, A. C. Sharrow, A. Wells, L. J. Robinson, and H. C. Blair Necessity of inositol (1,4,5)-trisphosphate receptor 1 and {micro}-calpain in NO-induced osteoclast motility J. Cell Sci., August 15, 2007; 120(16): 2884 - 2894. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Tsuboi Requirement for a Complex of Wiskott-Aldrich Syndrome Protein (WASP) with WASP Interacting Protein in Podosome Formation in Macrophages J. Immunol., March 1, 2007; 178(5): 2987 - 2995. [Abstract] [Full Text] [PDF]
|
|
