Spatiotemporal dynamics of actin-rich adhesion microdomains: influence of substrate flexibility

Collin, Olivier; Tracqui, Philippe; Stéphanou, Angélique; Usson, Yves; Clément-Lacroix, Jocelyne; Planus, Emmanuelle

doi:10.1242/jcs.02838

Cited by 96 publications

(83 citation statements)

References 69 publications

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“…Accordingly, inhibition of Erk activation by U0126 would slow podosome disassembly, resulting in the formation of interconnected actin-rich columns. It is noteworthy that podosome clusters in the form of rosettes have been observed in many different cell types including macrophages, osteoclasts, fibroblasts, endothelial cells, and RSV-transformed BHK21 cells [42,43,44,45,46,47]. To our knowledge, this is the first report of the formation of interconnected actin-rich columns in vascular smooth muscle cells.…”

Section: Discussionmentioning

confidence: 66%

Erk1/2 MAPK and caldesmon differentially regulate podosome dynamics in A7r5 vascular smooth muscle cells

Kordowska

Williams

et al. 2007

Experimental Cell Research

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We tested the hypothesis that the MEK/Erk/caldesmon phosphorylation cascade regulates PKCmediated podosome dynamics in A7r5 cells. We observed the phosphorylation of MEK, Erk and caldesmon, and their translocation to the podosomes upon phorbol dibutyrate (PDBu) stimulation, together with the nuclear translocation of phospho-MEK and phospho-Erk. After MEK inhibition by U0126, Erk translocated to the interconnected actin-rich columns but failed to translocate to the nucleus, suggesting that podosomes served as a site for Erk phosphorylation. The interconnected actin-rich columns in U0126-treated, PDBu-stimulated cells contained α-actinin, caldesmon, vinculin, and metalloproteinase-2. Caldesmon and vinculin became integrated with F-actin at the columns, in contrast to their typical location at the ring of podosomes. Live-imaging experiments suggested the growth of these columns from podosomes that were slow to disassemble. The observed modulation of podosome size and life time in A7r5 cells overexpressing wild-type and phosphorylation-deficient caldesmon-GFP mutants in comparison to untransfected cells suggests that caldesmon and caldesmon phosphorylation modulate podosome dynamics in A7r5 cells. These results suggest that Erk1/2 and caldesmon differentially modulate PKC-mediated formation and/or dynamics of podosomes in A7r5 vascular smooth muscle cells.

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Section: Discussionmentioning

confidence: 66%

Erk1/2 MAPK and caldesmon differentially regulate podosome dynamics in A7r5 vascular smooth muscle cells

Kordowska

Williams

et al. 2007

Experimental Cell Research

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“…In turn, cells adjust their internal stiffness to match that of their substrate (Solon et al, 2007). In fibroblasts, distribution and life span of podosomes is affected by substrate rigidity and increased stiffness favors the formation of individual podosomes (Collin et al, 2006). The chemical and mechanical properties of bone or bone-like matrix are likely to affect osteoclast adhesive properties by modifying Rho GTPases signaling cascades.…”

Section: Discussionmentioning

confidence: 99%

Rho GTPases in osteoclasts: Orchestrators of podosome arrangement

Ory

Brazier

Pawlak

et al. 2008

European Journal of Cell Biology

130

101

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Cells from the myeloid lineage, namely macrophages, dendritic cells and osteoclasts develop podosomes instead of stress fibers and focal adhesions to adhere and migrate.Podosomes share many components with focal adhesions but differ in their molecular organization, with a dense core of polymerized actin surrounded by scaffolding proteins, kinases and integrins. Podosomes are found either isolated both in macrophages and dendritic cells or arranged into superstructures in osteoclasts. When osteoclasts resorb bone, they form an F-actin rich sealing zone, which is a dense array of connected podosomes that firmly anchors osteoclasts to bone. It delineates a compartment in which protons and proteases are secreted to dissolve and degrade the mineralized matrix. Since Rho GTPases have been shown to control F-actin stress fibers and focal adhesions in mesenchymal cells, the question of whether they could also control podosome formation and arrangement in cells from the myeloid lineage, and particularly in osteoclasts, rapidly emerged. This article considers recent advances made in our understanding of podosome arrangements in osteoclasts and how Rho GTPases may control it.

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“…For instance, formation of podosomes was shown to involve (local) inhibition of myosin II in smooth muscle cells as well as neuroblastoma cells (Burgstaller and Gimona, 2004;Clark et al, 2006), whereas, in macrophages or fibroblasts (Collin et al, 2006), myosin-II-based activity is needed for the formation and maintenance of these structures.…”

Section: Discussionmentioning

confidence: 99%

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

Helden

Oud

Joosten

et al. 2008

Journal of Cell Science

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Podosomes are dynamic adhesion structures found in dendritic cells (DCs) and other cells of the myeloid lineage. We previously showed that prostaglandin E2 (PGE 2 ), 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 PGE 2 stimulation leads to activation of the small GTPase RhoA, decreased levels of Rac1-GTP and Cdc42-GTP are observed. These results show that PGE 2 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.Supplementary material available online at

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Spatiotemporal dynamics of actin-rich adhesion microdomains: influence of substrate flexibility

Cited by 96 publications

References 69 publications

Erk1/2 MAPK and caldesmon differentially regulate podosome dynamics in A7r5 vascular smooth muscle cells

Erk1/2 MAPK and caldesmon differentially regulate podosome dynamics in A7r5 vascular smooth muscle cells

Rho GTPases in osteoclasts: Orchestrators of podosome arrangement

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

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