ArticleMolecular biology of the cell2012
The Rho-guanine nucleotide exchange factor Trio controls leukocyte transendothelial migration by promoting docking structure formation.
Article in Molecular biology of the cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 81 citations in OpenAlex.
- Oxidized Phospholipids on Lipoprotein(a) Elicit Arterial Wall Inflammation and an Inflammatory Monocyte Response in Humans.Circulation · 2016Trial
- Neutrophil serine proteases degrade endothelial cortactin and promote extravasation.The Journal of cell biology · 2026Article
- Research Progress on the ARHGEF Family in Cardiovascular Diseases.Cell biochemistry and function · 2026Review
- Endothelial RhoGEF Trio is involved in angiogenesis.Vascular biology (Bristol, England) · 2026Article
- The Rho GEF Trio functions in contact inhibition of locomotion of neural crest cells by interacting with Ptk7.Development (Cambridge, England) · 2025Article
- Serine phosphorylation of the RhoGEF Trio stabilizes endothelial cell-cell junctions.Small GTPases · 2023Article
- Single-step genome-wide association analyses of claw horn lesions in Holstein cattle using linear and threshold models.Genetics, selection, evolution : GSE · 2023Article
- Low-Dose Azathioprine in Combination with Allopurinol: The Past, Present and Future of This Useful Duo.Digestive diseases and sciences · 2022Review
- Endothelial ARHGEF26 is an angiogenic factor promoting VEGF signalling.Cardiovascular research · 2022Article
- Autoinhibition of the GEF activity of cytoskeletal regulatory protein Trio is disrupted in neurodevelopmental disorder-related genetic variants.The Journal of biological chemistry · 2022Article
- Intercellular Adhesion Molecule-1 Enhances Myonuclear Transcription during Injury-Induced Muscle Regeneration.International journal of molecular sciences · 2022Article
- The RhoGEF Trio: A Protein with a Wide Range of Functions in the Vascular Endothelium.International journal of molecular sciences · 2021Review
- Identification of guanine nucleotide exchange factors that increase Cdc42 activity in primary human endothelial cells.Small GTPases · 2021Article
- Review
- Inflammation-Related Risk Loci in Genome-Wide Association Studies of Coronary Artery Disease.Cells · 2021Review
- Trio family proteins as regulators of cell migration and morphogenesis in development and disease - mechanisms and cellular contexts.Journal of cell science · 2021Review
- High Endothelial Venules Accelerate Naive T Cell Recruitment by Tumor Necrosis Factor-Mediated R-Ras Upregulation.The American journal of pathology · 2021Article
- Endothelial Focal Adhesions Are Functional Obstacles for Leukocytes During Basolateral Crawling.Frontiers in immunology · 2021Article
- Rho GTPase signalling networks in cancer cell transendothelial migration.Vascular biology (Bristol, England) · 2021Review
- Increasing spatial resolution of photoregulated GTPases through immobilized peripheral membrane proteins.Small GTPases · 2020Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Leukocyte transendothelial migration involves the active participation of the endothelium through the formation of apical membrane protrusions that embrace adherent leukocytes, termed docking structures. Using live-cell imaging, we find that prior to transmigration, endothelial docking structures form around 80% of all neutrophils. Previously we showed that endothelial RhoG and SGEF control leukocyte transmigration. In this study, our data reveal that both full-length Trio and the first DH-PH (TrioD1) domain of Trio, which can activate Rac1 and RhoG, interact with ICAM-1 and are recruited to leukocyte adhesion sites. Moreover, upon clustering of ICAM-1, the Rho-guanine nucleotide exchange factor Trio activates Rac1, prior to activating RhoG, in a filamin-dependent manner. We further show that docking structure formation is initiated by ICAM-1 clustering into ring-like structures, which is followed by apical membrane protrusion. Interestingly, we find that Rac1 is required for ICAM-1 clustering, whereas RhoG controls membrane protrusion formation. Finally, silencing endothelial Trio expression or reducing TrioD1 activity without affecting SGEF impairs both docking structure formation and leukocyte transmigration. We conclude that Trio promotes leukocyte transendothelial migration by inducing endothelial docking structure formation in a filamin-dependent manner through the activation of Rac1 and RhoG.
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