ArticleMolecular and cellular biology2003
Actin can reorganize into podosomes in aortic endothelial cells, a process controlled by Cdc42 and RhoA.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 1 of them a synthesis that pooled it.
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Who cites it
78 citing papers in PubMed, 1 synthesis or guideline pooled it, 194 citations in OpenAlex.
- Effects of theInternational journal of molecular sciences · 2021Pooled it
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- Unraveling the role of the WIPF1/ACTN4 complex in podosome formation of human placental EVTs: Insights into recurrent spontaneous abortion.Genes & diseases · 2025Article
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- Mechanomorphological Guidance of Colloidal Gel Regulates Cell Morphogenesis.Macromolecular bioscience · 2023Article
- ARHGAP17 regulates the spatiotemporal activity of Cdc42 at invadopodia.The Journal of cell biology · 2023Article
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- Baculovirus actin-rearrangement-inducing factor ARIF-1 induces the formation of dynamic invadosome clusters.Molecular biology of the cell · 2021Article
- Crosstalk between WIP and Rho family GTPases.Small GTPases · 2020Review
- Mechanical Cues Affect Migration and Invasion of Cells From Three Different Directions.Frontiers in cell and developmental biology · 2020Review
- Article
- Nck adapter proteins promote podosome biogenesis facilitating extracellular matrix degradation and cancer invasion.Cancer medicine · 2019Article
- Forces and constraints controlling podosome assembly and disassembly.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019Article
- Cause and effect of microenvironmental acidosis on bone metastases.Cancer metastasis reviews · 2019Review
- Hic-5 regulates Src-induced invadopodia rosette formation and organization.Molecular biology of the cell · 2019Article
18 more citing papers are in PubMed but not listed here.
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4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Members of the Rho GTPase family play a central role in the orchestration of cytoskeletal rearrangements, which are of prime importance in endothelial cell physiology. To explore their role in this specialized cell type, we used the bacterial toxin cytotoxic necrotizing factor 1 (CNF1) as a Rho GTPase activator. Punctate filamentous actin structures appeared along the ventral plasma membrane of endothelial cells and were identified as the core of podosomes by the distinctive vinculin ring around the F-actin. Rho, Rac, and Cdc42 were all identified as targets of CNF1, but only a constitutively active mutant of Cdc42 could substitute for CNF1 in podosome induction. Accordingly, organization of F-actin in these structures was highly dependent on the main Cdc42 cytoskeletal effector N-Wiskott-Aldrich syndrome protein. Other components of the actin machinery such as Arp2/3 and for the first time WIP also colocalized at these sites. Like CNF1 treatment, sustained Cdc42 activity induced a time-dependent F-actin-vinculin reorganization, prevented cytokinesis, and downregulated Rho activity. Finally, podosomes were also detected on endothelial cells explanted from patients undergoing cardiac surgery. These data provide the first description of podosomes in endothelial cells. The identification of such specialized structures opens up a new field of investigation in terms of endothelium pathophysiology.
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