The Experts below are selected from a list of 5109 Experts worldwide ranked by ideXlab platform
Elisabeth Génot - One of the best experts on this subject based on the ideXlab platform.
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Variations on the theme of podosomes: A matter of context.
Biochimica et Biophysica Acta, 2018Co-Authors: Florian Alonso, Pirjo Spuul, Ïjsbrand M. Kramer, Thomas Daubon, Elisabeth GénotAbstract:Abstract Extensive in vitro studies have described podosomes as Actin-Based Structures at the plasma membrane, connecting the cell with its extracellular matrix and endowed with multiple capabilities. Contractile Actin-myosin cables assemble them into a network that constitutes a multifaceted cellular superstructure taking different forms – with common characteristics – but manifesting different properties depending on the context of study. Their morphology and their role in cell functioning and behavior are therefore now apprehended in in vivo or in vitro situations relevant to physiological processes. We focus here on three of them, namely: macrophage migration, antigen presentation by dendritic cells and endothelial cell sprouting during angiogenesis to highlight the characteristics of podosomes and their functioning shaped by the microenvironment.
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Sodium fluoride induces podosome formation in endothelial cells.
Biology of the cell, 2010Co-Authors: Florence Tatin, Elisabeth Génot, Edith Reuzeau, Florence Grise, Violaine MoreauAbstract:Background information. Fluoride is a well-known G-protein activator. Exposure of cultured cells to its derivatives results in Actin cytoskeleton remodelling. Podosomes are Actin-Based Structures endowed with adhesion and matrix-degradation functions. This study investigates Actin cytoskeleton reorganization induced by fluoride in endothelial cells. Results. Treatment of cultured endothelial cells with sodium fluoride (NaF) results in a rapid and potent stimulation of podosome formation. Furthermore, we show that Cdc42 (cell-division cycle 42), Rac1 and RhoA activities are stimulated in NaF-treated cells. However, podosome assembly is dependent on Cdc42 and Rac1, but not RhoA. Although the sole activation of Cdc42 is sufficient to induce individual podosomes, a balance between RhoGTPase activities regulates podosome formation in response to NaF, which in this case are often found in groups or rosettes. As in other models, podosome formation in endothelial cells exposed to NaF also involves Src. Finally, we demonstrate that NaF-induced podosomes are fully competent for matrix protein degradation. Conclusions. Taken together, our findings establish NaF as a novel inducer of podosomes in endothelial cells in vitro.
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Transforming Growth Factor β Induces Rosettes of Podosomes in Primary Aortic Endothelial Cells
Molecular and cellular biology, 2006Co-Authors: Christine Varon, Ïjsbrand M. Kramer, Violaine Moreau, Florence Tatin, Ellen Van Obberghen-schilling, Samantha Fernandez-sauze, Edith Reuzeau, Elisabeth GénotAbstract:Cytoskeletal rearrangements are central to endothelial cell physiology and are controlled by soluble factors, matrix proteins, cell-cell interactions, and mechanical forces. We previously reported that aortic endothelial cells can rearrange their cytoskeletons into complex Actin-Based Structures called podosomes when a constitutively active mutant of Cdc42 is expressed. We now report that transforming growth factor beta (TGF-β) promotes podosome formation in primary aortic endothelial cells. TGF-β-induced podosomes assembled together into large ring- or crescent-shaped Structures. Their formation was dependent on protein synthesis and required functional Src, phosphatidylinositide 3-kinase, Cdc42, RhoA, and Smad signaling. MT1-MMP and metalloprotease 9 (MMP9), both upregulated by TGF-β, were detected at sites of podosome formation, and MT1-MMP was found to be involved in the local degradation of extracellular matrix proteins beneath the podosomes and required for the invasion of collagen gels by endothelial cells. We propose that TGF-β plays an important role in endothelial cell physiology by inducing the formation of podosomal Structures endowed with metalloprotease activity that may contribute to arterial remodeling.
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Transforming growth factor beta induces rosettes of podosomes in primary aortic endothelial cells.
Molecular and Cellular Biology, 2006Co-Authors: Christine Varon, Violaine Moreau, Florence Tatin, Ellen Van Obberghen-schilling, Samantha Fernandez-sauze, Edith Reuzeau, Ijsbrand Kramer, Elisabeth GénotAbstract:Cytoskeletal rearrangements are central to endothelial cell physiology and are controlled by soluble factors, matrix proteins, cell-cell interactions, and mechanical forces. We previously reported that aortic endothelial cells can rearrange their cytoskeletons into complex Actin-Based Structures called podosomes when a constitutively active mutant of Cdc42 is expressed. We now report that transforming growth factor beta (TGF-beta) promotes podosome formation in primary aortic endothelial cells. TGF-beta-induced podosomes assembled together into large ring- or crescent-shaped Structures. Their formation was dependent on protein synthesis and required functional Src, phosphatidylinositide 3-kinase, Cdc42, RhoA, and Smad signaling. MT1-MMP and metalloprotease 9 (MMP9), both upregulated by TGF-beta, were detected at sites of podosome formation, and MT1-MMP was found to be involved in the local degradation of extracellular matrix proteins beneath the podosomes and required for the invasion of collagen gels by endothelial cells. We propose that TGF-beta plays an important role in endothelial cell physiology by inducing the formation of podosomal Structures endowed with metalloprotease activity that may contribute to arterial remodeling.
Violaine Moreau - One of the best experts on this subject based on the ideXlab platform.
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The microenvironment controls invadosome plasticity.
Journal of cell science, 2016Co-Authors: Julie Di Martino, Elodie Henriet, Zakaria Ezzoukhry, Jacky G. Goetz, Violaine Moreau, Frédéric SaltelAbstract:Invadosomes are Actin-Based Structures involved in extracellular matrix degradation. Invadosomes is a term that includes podosomes and invadopodia, which decorate normal and tumour cells, respectively. They are mainly organised into dots or rosettes, and podosomes and invadopodia are often compared and contrasted. Various internal or external stimuli have been shown to induce their formation and/or activity. In this Commentary, we address the impact of the microenvironment and the role of matrix receptors on the formation, and dynamic and degradative activities of invadosomes. In particular, we highlight recent findings regarding the role of type I collagen fibrils in inducing the formation of a new linear organisation of invadosomes. We will also discuss invadosome plasticity more generally and emphasise its physio-pathological relevance.
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Cdc42 and Tks5: A minimal and universal molecular signature for functional invadosomes
Cell adhesion & migration, 2014Co-Authors: Julie Di Martino, Frédéric Saltel, Lisa Paysan, Caroline Gest, Valérie Lagrée, Amélie Juin, Violaine MoreauAbstract:Invadosomes are Actin-Based Structures involved in extracellular-matrix degradation. Invadosomes, either known as podosomes or invadopodia, are found in an increasing number of cell types. Moreover, their overall organization and molecular composition may vary from one cell type to the other. Some are constitutive such as podosomes in hematopoietic cells whereas others are inducible. However, they share the same feature, their ability to interact and to degrade the extracellular matrix. Based on the literature and our own experiments, the aim of this study was to establish a minimal molecular definition of active invadosomes. We first highlighted that Cdc42 is the key RhoGTPase involved in invadosome formation in all described models. Using different cellular models, such as NIH-3T3, HeLa, and endothelial cells, we demonstrated that overexpression of an active form of Cdc42 is sufficient to form invadosome Actin cores. Therefore, active Cdc42 must be considered not only as an inducer of filopodia, but als...
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Sodium fluoride induces podosome formation in endothelial cells.
Biology of the cell, 2010Co-Authors: Florence Tatin, Elisabeth Génot, Edith Reuzeau, Florence Grise, Violaine MoreauAbstract:Background information. Fluoride is a well-known G-protein activator. Exposure of cultured cells to its derivatives results in Actin cytoskeleton remodelling. Podosomes are Actin-Based Structures endowed with adhesion and matrix-degradation functions. This study investigates Actin cytoskeleton reorganization induced by fluoride in endothelial cells. Results. Treatment of cultured endothelial cells with sodium fluoride (NaF) results in a rapid and potent stimulation of podosome formation. Furthermore, we show that Cdc42 (cell-division cycle 42), Rac1 and RhoA activities are stimulated in NaF-treated cells. However, podosome assembly is dependent on Cdc42 and Rac1, but not RhoA. Although the sole activation of Cdc42 is sufficient to induce individual podosomes, a balance between RhoGTPase activities regulates podosome formation in response to NaF, which in this case are often found in groups or rosettes. As in other models, podosome formation in endothelial cells exposed to NaF also involves Src. Finally, we demonstrate that NaF-induced podosomes are fully competent for matrix protein degradation. Conclusions. Taken together, our findings establish NaF as a novel inducer of podosomes in endothelial cells in vitro.
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Transforming Growth Factor β Induces Rosettes of Podosomes in Primary Aortic Endothelial Cells
Molecular and cellular biology, 2006Co-Authors: Christine Varon, Ïjsbrand M. Kramer, Violaine Moreau, Florence Tatin, Ellen Van Obberghen-schilling, Samantha Fernandez-sauze, Edith Reuzeau, Elisabeth GénotAbstract:Cytoskeletal rearrangements are central to endothelial cell physiology and are controlled by soluble factors, matrix proteins, cell-cell interactions, and mechanical forces. We previously reported that aortic endothelial cells can rearrange their cytoskeletons into complex Actin-Based Structures called podosomes when a constitutively active mutant of Cdc42 is expressed. We now report that transforming growth factor beta (TGF-β) promotes podosome formation in primary aortic endothelial cells. TGF-β-induced podosomes assembled together into large ring- or crescent-shaped Structures. Their formation was dependent on protein synthesis and required functional Src, phosphatidylinositide 3-kinase, Cdc42, RhoA, and Smad signaling. MT1-MMP and metalloprotease 9 (MMP9), both upregulated by TGF-β, were detected at sites of podosome formation, and MT1-MMP was found to be involved in the local degradation of extracellular matrix proteins beneath the podosomes and required for the invasion of collagen gels by endothelial cells. We propose that TGF-β plays an important role in endothelial cell physiology by inducing the formation of podosomal Structures endowed with metalloprotease activity that may contribute to arterial remodeling.
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Transforming growth factor beta induces rosettes of podosomes in primary aortic endothelial cells.
Molecular and Cellular Biology, 2006Co-Authors: Christine Varon, Violaine Moreau, Florence Tatin, Ellen Van Obberghen-schilling, Samantha Fernandez-sauze, Edith Reuzeau, Ijsbrand Kramer, Elisabeth GénotAbstract:Cytoskeletal rearrangements are central to endothelial cell physiology and are controlled by soluble factors, matrix proteins, cell-cell interactions, and mechanical forces. We previously reported that aortic endothelial cells can rearrange their cytoskeletons into complex Actin-Based Structures called podosomes when a constitutively active mutant of Cdc42 is expressed. We now report that transforming growth factor beta (TGF-beta) promotes podosome formation in primary aortic endothelial cells. TGF-beta-induced podosomes assembled together into large ring- or crescent-shaped Structures. Their formation was dependent on protein synthesis and required functional Src, phosphatidylinositide 3-kinase, Cdc42, RhoA, and Smad signaling. MT1-MMP and metalloprotease 9 (MMP9), both upregulated by TGF-beta, were detected at sites of podosome formation, and MT1-MMP was found to be involved in the local degradation of extracellular matrix proteins beneath the podosomes and required for the invasion of collagen gels by endothelial cells. We propose that TGF-beta plays an important role in endothelial cell physiology by inducing the formation of podosomal Structures endowed with metalloprotease activity that may contribute to arterial remodeling.
Florence Tatin - One of the best experts on this subject based on the ideXlab platform.
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Sodium fluoride induces podosome formation in endothelial cells.
Biology of the cell, 2010Co-Authors: Florence Tatin, Elisabeth Génot, Edith Reuzeau, Florence Grise, Violaine MoreauAbstract:Background information. Fluoride is a well-known G-protein activator. Exposure of cultured cells to its derivatives results in Actin cytoskeleton remodelling. Podosomes are Actin-Based Structures endowed with adhesion and matrix-degradation functions. This study investigates Actin cytoskeleton reorganization induced by fluoride in endothelial cells. Results. Treatment of cultured endothelial cells with sodium fluoride (NaF) results in a rapid and potent stimulation of podosome formation. Furthermore, we show that Cdc42 (cell-division cycle 42), Rac1 and RhoA activities are stimulated in NaF-treated cells. However, podosome assembly is dependent on Cdc42 and Rac1, but not RhoA. Although the sole activation of Cdc42 is sufficient to induce individual podosomes, a balance between RhoGTPase activities regulates podosome formation in response to NaF, which in this case are often found in groups or rosettes. As in other models, podosome formation in endothelial cells exposed to NaF also involves Src. Finally, we demonstrate that NaF-induced podosomes are fully competent for matrix protein degradation. Conclusions. Taken together, our findings establish NaF as a novel inducer of podosomes in endothelial cells in vitro.
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Transforming Growth Factor β Induces Rosettes of Podosomes in Primary Aortic Endothelial Cells
Molecular and cellular biology, 2006Co-Authors: Christine Varon, Ïjsbrand M. Kramer, Violaine Moreau, Florence Tatin, Ellen Van Obberghen-schilling, Samantha Fernandez-sauze, Edith Reuzeau, Elisabeth GénotAbstract:Cytoskeletal rearrangements are central to endothelial cell physiology and are controlled by soluble factors, matrix proteins, cell-cell interactions, and mechanical forces. We previously reported that aortic endothelial cells can rearrange their cytoskeletons into complex Actin-Based Structures called podosomes when a constitutively active mutant of Cdc42 is expressed. We now report that transforming growth factor beta (TGF-β) promotes podosome formation in primary aortic endothelial cells. TGF-β-induced podosomes assembled together into large ring- or crescent-shaped Structures. Their formation was dependent on protein synthesis and required functional Src, phosphatidylinositide 3-kinase, Cdc42, RhoA, and Smad signaling. MT1-MMP and metalloprotease 9 (MMP9), both upregulated by TGF-β, were detected at sites of podosome formation, and MT1-MMP was found to be involved in the local degradation of extracellular matrix proteins beneath the podosomes and required for the invasion of collagen gels by endothelial cells. We propose that TGF-β plays an important role in endothelial cell physiology by inducing the formation of podosomal Structures endowed with metalloprotease activity that may contribute to arterial remodeling.
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Transforming growth factor beta induces rosettes of podosomes in primary aortic endothelial cells.
Molecular and Cellular Biology, 2006Co-Authors: Christine Varon, Violaine Moreau, Florence Tatin, Ellen Van Obberghen-schilling, Samantha Fernandez-sauze, Edith Reuzeau, Ijsbrand Kramer, Elisabeth GénotAbstract:Cytoskeletal rearrangements are central to endothelial cell physiology and are controlled by soluble factors, matrix proteins, cell-cell interactions, and mechanical forces. We previously reported that aortic endothelial cells can rearrange their cytoskeletons into complex Actin-Based Structures called podosomes when a constitutively active mutant of Cdc42 is expressed. We now report that transforming growth factor beta (TGF-beta) promotes podosome formation in primary aortic endothelial cells. TGF-beta-induced podosomes assembled together into large ring- or crescent-shaped Structures. Their formation was dependent on protein synthesis and required functional Src, phosphatidylinositide 3-kinase, Cdc42, RhoA, and Smad signaling. MT1-MMP and metalloprotease 9 (MMP9), both upregulated by TGF-beta, were detected at sites of podosome formation, and MT1-MMP was found to be involved in the local degradation of extracellular matrix proteins beneath the podosomes and required for the invasion of collagen gels by endothelial cells. We propose that TGF-beta plays an important role in endothelial cell physiology by inducing the formation of podosomal Structures endowed with metalloprotease activity that may contribute to arterial remodeling.
Edith Reuzeau - One of the best experts on this subject based on the ideXlab platform.
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Sodium fluoride induces podosome formation in endothelial cells.
Biology of the cell, 2010Co-Authors: Florence Tatin, Elisabeth Génot, Edith Reuzeau, Florence Grise, Violaine MoreauAbstract:Background information. Fluoride is a well-known G-protein activator. Exposure of cultured cells to its derivatives results in Actin cytoskeleton remodelling. Podosomes are Actin-Based Structures endowed with adhesion and matrix-degradation functions. This study investigates Actin cytoskeleton reorganization induced by fluoride in endothelial cells. Results. Treatment of cultured endothelial cells with sodium fluoride (NaF) results in a rapid and potent stimulation of podosome formation. Furthermore, we show that Cdc42 (cell-division cycle 42), Rac1 and RhoA activities are stimulated in NaF-treated cells. However, podosome assembly is dependent on Cdc42 and Rac1, but not RhoA. Although the sole activation of Cdc42 is sufficient to induce individual podosomes, a balance between RhoGTPase activities regulates podosome formation in response to NaF, which in this case are often found in groups or rosettes. As in other models, podosome formation in endothelial cells exposed to NaF also involves Src. Finally, we demonstrate that NaF-induced podosomes are fully competent for matrix protein degradation. Conclusions. Taken together, our findings establish NaF as a novel inducer of podosomes in endothelial cells in vitro.
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Transforming Growth Factor β Induces Rosettes of Podosomes in Primary Aortic Endothelial Cells
Molecular and cellular biology, 2006Co-Authors: Christine Varon, Ïjsbrand M. Kramer, Violaine Moreau, Florence Tatin, Ellen Van Obberghen-schilling, Samantha Fernandez-sauze, Edith Reuzeau, Elisabeth GénotAbstract:Cytoskeletal rearrangements are central to endothelial cell physiology and are controlled by soluble factors, matrix proteins, cell-cell interactions, and mechanical forces. We previously reported that aortic endothelial cells can rearrange their cytoskeletons into complex Actin-Based Structures called podosomes when a constitutively active mutant of Cdc42 is expressed. We now report that transforming growth factor beta (TGF-β) promotes podosome formation in primary aortic endothelial cells. TGF-β-induced podosomes assembled together into large ring- or crescent-shaped Structures. Their formation was dependent on protein synthesis and required functional Src, phosphatidylinositide 3-kinase, Cdc42, RhoA, and Smad signaling. MT1-MMP and metalloprotease 9 (MMP9), both upregulated by TGF-β, were detected at sites of podosome formation, and MT1-MMP was found to be involved in the local degradation of extracellular matrix proteins beneath the podosomes and required for the invasion of collagen gels by endothelial cells. We propose that TGF-β plays an important role in endothelial cell physiology by inducing the formation of podosomal Structures endowed with metalloprotease activity that may contribute to arterial remodeling.
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Transforming growth factor beta induces rosettes of podosomes in primary aortic endothelial cells.
Molecular and Cellular Biology, 2006Co-Authors: Christine Varon, Violaine Moreau, Florence Tatin, Ellen Van Obberghen-schilling, Samantha Fernandez-sauze, Edith Reuzeau, Ijsbrand Kramer, Elisabeth GénotAbstract:Cytoskeletal rearrangements are central to endothelial cell physiology and are controlled by soluble factors, matrix proteins, cell-cell interactions, and mechanical forces. We previously reported that aortic endothelial cells can rearrange their cytoskeletons into complex Actin-Based Structures called podosomes when a constitutively active mutant of Cdc42 is expressed. We now report that transforming growth factor beta (TGF-beta) promotes podosome formation in primary aortic endothelial cells. TGF-beta-induced podosomes assembled together into large ring- or crescent-shaped Structures. Their formation was dependent on protein synthesis and required functional Src, phosphatidylinositide 3-kinase, Cdc42, RhoA, and Smad signaling. MT1-MMP and metalloprotease 9 (MMP9), both upregulated by TGF-beta, were detected at sites of podosome formation, and MT1-MMP was found to be involved in the local degradation of extracellular matrix proteins beneath the podosomes and required for the invasion of collagen gels by endothelial cells. We propose that TGF-beta plays an important role in endothelial cell physiology by inducing the formation of podosomal Structures endowed with metalloprotease activity that may contribute to arterial remodeling.
Christine Varon - One of the best experts on this subject based on the ideXlab platform.
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Transforming Growth Factor β Induces Rosettes of Podosomes in Primary Aortic Endothelial Cells
Molecular and cellular biology, 2006Co-Authors: Christine Varon, Ïjsbrand M. Kramer, Violaine Moreau, Florence Tatin, Ellen Van Obberghen-schilling, Samantha Fernandez-sauze, Edith Reuzeau, Elisabeth GénotAbstract:Cytoskeletal rearrangements are central to endothelial cell physiology and are controlled by soluble factors, matrix proteins, cell-cell interactions, and mechanical forces. We previously reported that aortic endothelial cells can rearrange their cytoskeletons into complex Actin-Based Structures called podosomes when a constitutively active mutant of Cdc42 is expressed. We now report that transforming growth factor beta (TGF-β) promotes podosome formation in primary aortic endothelial cells. TGF-β-induced podosomes assembled together into large ring- or crescent-shaped Structures. Their formation was dependent on protein synthesis and required functional Src, phosphatidylinositide 3-kinase, Cdc42, RhoA, and Smad signaling. MT1-MMP and metalloprotease 9 (MMP9), both upregulated by TGF-β, were detected at sites of podosome formation, and MT1-MMP was found to be involved in the local degradation of extracellular matrix proteins beneath the podosomes and required for the invasion of collagen gels by endothelial cells. We propose that TGF-β plays an important role in endothelial cell physiology by inducing the formation of podosomal Structures endowed with metalloprotease activity that may contribute to arterial remodeling.
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Transforming growth factor beta induces rosettes of podosomes in primary aortic endothelial cells.
Molecular and Cellular Biology, 2006Co-Authors: Christine Varon, Violaine Moreau, Florence Tatin, Ellen Van Obberghen-schilling, Samantha Fernandez-sauze, Edith Reuzeau, Ijsbrand Kramer, Elisabeth GénotAbstract:Cytoskeletal rearrangements are central to endothelial cell physiology and are controlled by soluble factors, matrix proteins, cell-cell interactions, and mechanical forces. We previously reported that aortic endothelial cells can rearrange their cytoskeletons into complex Actin-Based Structures called podosomes when a constitutively active mutant of Cdc42 is expressed. We now report that transforming growth factor beta (TGF-beta) promotes podosome formation in primary aortic endothelial cells. TGF-beta-induced podosomes assembled together into large ring- or crescent-shaped Structures. Their formation was dependent on protein synthesis and required functional Src, phosphatidylinositide 3-kinase, Cdc42, RhoA, and Smad signaling. MT1-MMP and metalloprotease 9 (MMP9), both upregulated by TGF-beta, were detected at sites of podosome formation, and MT1-MMP was found to be involved in the local degradation of extracellular matrix proteins beneath the podosomes and required for the invasion of collagen gels by endothelial cells. We propose that TGF-beta plays an important role in endothelial cell physiology by inducing the formation of podosomal Structures endowed with metalloprotease activity that may contribute to arterial remodeling.
