1. Induction of transient macroapertures in endothelial cells through RhoA inhibition by Staphylococcus aureus factors
- Author
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Pierre Gounon, Céline Pulcini, Patrick Munro, Luce Landraud, René L. Clément, Olivier Dussurget, Emmanuel Lemichez, Amel Mettouchi, Gilles Flatau, Anne Doye, Monica Rolando, Michel R. Popoff, Laurent Boyer, Lemichez, Emmanuel, Toxines bactériennes dans la relation hôtes-pathogènes, Université Nice Sophia Antipolis (1965 - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-IFR50-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Côte d'Azur (UCA), Centre Commun de Microscopie Appliquée (CCMA), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA), Bactéries anaérobies et Toxines, Institut Pasteur [Paris] (IP), Biologie et physiopathologie cutanées : expression génique, signalisation et thérapie, COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-IFR50-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire central de bactériologie, Centre Hospitalier Universitaire de Nice (CHU Nice)-Hôpital l'Archet, Interactions Bactéries-Cellules (UIBC), Institut National de la Recherche Agronomique (INRA)-Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR50-Université Côte d'Azur (UCA)-Université Nice Sophia Antipolis (... - 2019) (UNS), Université Nice Sophia Antipolis (... - 2019) (UNS), Institut Pasteur [Paris], Institut National de la Recherche Agronomique (INRA)-Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Côte d'Azur (UCA)-Université Côte d'Azur (UCA)-IFR50-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Côte d'Azur (UCA)-Université Côte d'Azur (UCA), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Pasteur [Paris]-Institut National de la Recherche Agronomique (INRA)
- Subjects
RHOA ,MESH: ADP Ribose Transferases ,Epidermal cell differentiation ,MESH: Research Support, Non-U.S. Gov't ,MESH: Recombinant Proteins ,0302 clinical medicine ,MESH: Staphylococcus aureus ,Immunology and Allergy ,MESH: Endothelial Cells ,Transcellular ,Non-U.S. Gov't ,Cytoskeleton ,MESH: Bacterial Proteins ,Research Articles ,Cells, Cultured ,ADP Ribose Transferases ,0303 health sciences ,Gene knockdown ,Cultured ,biology ,030302 biochemistry & molecular biology ,Recombinant Proteins ,Cell biology ,[SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology ,medicine.anatomical_structure ,RNA Interference ,MESH: Cells, Cultured ,Staphylococcus aureus ,MESH: rhoA GTP-Binding Protein ,Endothelium ,Cells ,Immunology ,Molecular Sequence Data ,MESH: RNA Interference ,macromolecular substances ,Research Support ,Article ,03 medical and health sciences ,Bacterial Proteins ,medicine ,Humans ,[SDV.MP] Life Sciences [q-bio]/Microbiology and Parasitology ,Actin ,030304 developmental biology ,Basement membrane ,MESH: Humans ,MESH: Molecular Sequence Data ,Endothelial Cells ,Cell Biology ,biology.protein ,rhoA GTP-Binding Protein ,030217 neurology & neurosurgery - Abstract
The GTPase RhoA is a major regulator of the assembly of actin stress fibers and the contractility of the actomyosin cytoskeleton. The epidermal cell differentiation inhibitor (EDIN) and EDIN-like ADP-ribosyltransferases of Staphylococcus aureus catalyze the inactivation of RhoA, producing actin cable disruption. We report that purified recombinant EDIN and EDIN-producing S. aureus provoke large transcellular tunnels in endothelial cells that we have named macroapertures (MAs). These structures open transiently, followed by the appearance of actin-containing membrane waves extending over the aperture. Disruption of actin cables, either directly or indirectly, through rhoA RNAi knockdown also triggers the formation of MAs. Intoxication of endothelial monolayers by EDIN produces a loss of barrier function and provides direct access of the endothelium basement membrane to S. aureus.
- Published
- 2006