12 results on '"Tania Durré"'
Search Results
2. uPARAP/Endo180 receptor is a gatekeeper of VEGFR-2/VEGFR-3 heterodimerisation during pathological lymphangiogenesis
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Tania Durré, Florent Morfoisse, Charlotte Erpicum, Marie Ebroin, Silvia Blacher, Melissa García-Caballero, Christophe Deroanne, Thomas Louis, Cédric Balsat, Maureen Van de Velde, Seppo Kaijalainen, Frédéric Kridelka, Lars Engelholm, Ingrid Struman, Kari Alitalo, Niels Behrendt, Jenny Paupert, and Agnès Noel
- Subjects
Science - Abstract
VEGF-C drives lymphangiogenesis through binding to its receptors VEGFR-2 and VEGFR-3. Here, Durré et al. identify uPARAP/Endo180 as a critical regulator of VEGFR-2/VEGFR-3 heterodimerisation and downstream signaling in response to VEGF-C, and show that uPARAP deletion leads to the formation of hyperbranched vasculatures in pathological conditions.
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- 2018
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3. Contralateral Vascularized Lymph Node Transfer: An Optimized Mouse Model
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Giulia Virginia Vottero, Florent Morfoisse, Tania Durré, Silvia Blacher, Guillaume Becker, Mohamed A. Bahri, Alain Plenevaux, Agnès Noel, and Jean Luc Nizet
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lymphedema ,mouse model ,vascularized lymph node transfer ,Surgery ,RD1-811 - Abstract
Background Vascularized lymph node transfer (VLNT) is one of the surgical options in the treatment of lymphedema, but its mechanism of action has not yet been firmly clarified. In the VLNT mouse models described so far, the lymph node flap is performed between two different sites in the same lymphedematous paw. In this study, we describe an optimized VLNT mouse model using the contralateral paw as donor site, thus removing the bias of transferring a lymph node already damaged by irradiation and/or surgery required to induce lymphedema. Methods A lymphedema was induced on the left posterior paw in four experimental groups of mice (n = 8). Two weeks later, group 1 was the sham one, group 2 underwent a VLNT from the right inguinal region to the left, in group 3 a vascular endothelial growth factor (VEGF)-C sponge was placed alone in the left inguinal region, and in group 4 a VEGF-C sponge was associated to the VLNT. The 32 mice were followed during 3 months. Outcomes included paws volume, skin quality, inflammation in the lymphedematous tissue, and lymphatic network density and function. Results Group 4 displayed significantly higher (p
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- 2019
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4. Mesenchymal Stem Cells Shed Amphiregulin at the Surface of Lung Carcinoma Cells in a Juxtacrine Manner
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Oriane Carnet, Julie Lecomte, Anne Masset, Irina Primac, Tania Durré, Ludovic Maertens, Benoit Detry, Silvia Blacher, Christine Gilles, Christel Péqueux, Jenny Paupert, Jean-Michel Foidart, Guy Jerusalem, Didier Cataldo, and Agnès Noel
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Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,RC254-282 - Abstract
Solid tumors comprise cancer cells and different supportive stromal cells, including mesenchymal stem cells (MSCs), which have recently been shown to enhance tumor growth and metastasis. We provide new mechanistic insights into how bone marrow (BM)–derived MSCs co-injected with Lewis lung carcinoma cells promote tumor growth and metastasis in mice. The proinvasive effect of BM-MSCs exerted on tumor cells relies on an unprecedented juxtacrine action of BM-MSC, leading to the trans-shedding of amphiregulin (AREG) from the tumor cell membrane by tumor necrosis factor-α–converting enzyme carried by the BM-MSC plasma membrane. The released soluble AREG activates cancer cells and promotes their invasiveness. This novel concept is supported by the exploitation of different 2D and 3D culture systems and by pharmacological approaches using a tumor necrosis factor-α–converting enzyme inhibitor and AREG-blocking antibodies. Altogether, we here assign a new function to BM-MSC in tumor progression and establish an uncovered link between AREG and BM-MSC.
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- 2015
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5. Periostin in lymph node pre-metastatic niches governs lymphatic endothelial cell functions and metastatic colonization
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Lionel Gillot, Alizée Lebeau, Louis Baudin, Charles Pottier, Thomas Louis, Tania Durré, Rémi Longuespée, Gabriel Mazzucchelli, Christophe Nizet, Silvia Blacher, Frédéric Kridelka, and Agnès Noël
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Pharmacology ,Proteomics ,Vascular Endothelial Growth Factor C ,Endothelial Cells ,Uterine Cervical Neoplasms ,Cell Biology ,Cellular and Molecular Neuroscience ,Mice ,Lymphatic Metastasis ,Molecular Medicine ,Animals ,Humans ,Female ,Lymph Nodes ,Molecular Biology ,Cell Adhesion Molecules - Abstract
Although lymph node (LN) metastasis is an important prognostic parameter in cervical cancer, the tissue remodeling at a pre-metastatic state is poorly documented in LNs. We here identified periostin (POSTN) as a component of non-metastatic LNs by applying proteomic analyses and computerized image quantifications on LNs of patients with cervical cancer. We provide evidence for remarkable modifications of POSTN and lymphatic vessel distributions and densities in non-metastatic sentinel and metastatic human LNs, when compared to distant non-metastatic LNs. POSTN deposition at a pre-metastatic stage was demonstrated in a pre-clinical murine model (the ear sponge assay). Its expression by fibroblastic LN cells was assessed by in situ hybridization and in vitro cultures. In vitro, POSTN promoted lymphatic endothelial cell functions and tumor cell proliferation. Accordingly, the in vivo injection of recombinant POSTN together with VEGF-C boosted the lymphangiogenic response, while the metastatic potential of tumor cells was drastically reduced using a POSTN blocking antibody. This translational study also supports the existence of an unprecedented dialog “in cascade”, between the primary tumor and the first pelvic nodal relay in early cervical cancer, and subsequently from pelvic LN to para-aortic LNs in locally advanced cervical cancers. Collectively, this work highlights the association of POSTN deposition with lymphangiogenesis in LNs, and provides evidence for a key contribution of POSTN in promoting VEGF-C driven lymphangiogenesis and the seeding of metastatic cells.
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- 2021
6. Lipid Droplets Degradation by Autophagy Connects Mitochondria Metabolism to PROX1-driven Expression of Lymphatic Genes and Lymphangiogenesis
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Odeta Mece, Diede Houbaert, Tania Durré, Hannelore Maes, Marco Schaaf, Sanket More, Maarten Ganne, Melissa García-Caballero, Mila Borri, Jelle Verhoeven, Silvia Blacher, Bart Ghesquière, Mieke Dewerchin, Johannes Swinnen, Stefan Vinckier, Maria Soengas, Peter Carmeliet, Agnès Noel, and Patrizia Agostinis
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fungi ,sense organs - Abstract
Autophagy has an emerging vasculoprotective role but whether and how it regulates lymphatic endothelial cells (LEC) and lymphangiogenesis is unknown. Here, we show that genetic deficiency of autophagy in LEC impairs the responses to VEGF-C and injury-driven corneal lymphangiogenesis. Loss of autophagy compromises expression of lymphatic markers, affects mitochondrial dynamics and causes an accumulation of lipid droplets (LDs) in LEC and lymphatic vessels in vivo. When LDs accumulate because lipophagy is impaired, mitochondrial ATP production, fatty acid oxidation (FAO), acetyl-CoA/CoA ratio and expression of lymphangiogenic PROX1 target genes are dwindled. Enforcing mitochondria fusion by silencing dynamin-related-protein 1 (DRP1) in autophagy-deficient LEC fails to affect LDs turnover and lymphatic gene expression, whereas supplementing the acetyl-CoA precursor acetate rescues LEC identity and lymphangiogenesis in LEC-Atg5-/- mice. Our findings reveal that lipophagy in LEC by supporting FAO, preserves a mitochondrial-PROX1 gene expression circuit that ensures LEC identity, responsiveness to lymphangiogenic mediators and lymphangiogenesis.
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- 2021
7. Tumor exposed-lymphatic endothelial cells promote primary tumor growth via IL6
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Maureen, Van de Velde, Marie, Ebroin, Tania, Durré, Marc, Joiret, Lionel, Gillot, Silvia, Blacher, Liesbet, Geris, Frédéric, Kridelka, and Agnès, Noel
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Skin Neoplasms ,Neovascularization, Pathologic ,Interleukin-6 ,Endothelial Cells ,Mice, Nude ,Apoptosis ,Ear ,Original Articles ,Xenograft Model Antitumor Assays ,Lymphatic endothelial cells ,Mice ,Tumor microenvironment ,Cell Movement ,Tumor Cells, Cultured ,Animals ,Humans ,Neoplasm Invasiveness ,sense organs ,Endothelial cell plasticity ,Lymphangiogenesis ,CAF ,Cell Proliferation - Abstract
Solid tumors are composed of tumor cells and stromal cells including lymphatic endothelial cells (LEC), which are mainly viewed as cells forming lymphatic vessels involved in the transport of metastatic and immune cells. We here reveal a new mechanism by which tumor exposed-LEC (teLEC) exert mitogenic effects on tumor cells. Our conclusions are supported by morphological and molecular changes induced in teLEC that in turn enhance cancer cell invasion in 3D cultures and tumor cell proliferation in vivo. The characterization of teLEC secretome by RNA-Sequencing and cytokine array revealed that interleukine-6 (IL6) is one of the most modulated molecules in teLEC, whose production was negligible in unexposed LEC. Notably, neutralizing anti-human IL6 antibody abrogated teLEC-mediated mitogenic effects in vivo, when LEC were mixed with tumor cells in the ear sponge assay. We here assign a novel function to teLEC that is beyond their role of lymphatic vessel formation. This work highlights a new paradigm, in which teLEC exert “fibroblast-like properties”, contribute in a paracrine manner to the control of tumor cell properties and are worth considering as key stromal determinant in future studies., Highlights • teLEC, but not normal LEC, produce huge amount of IL6. • IL6-derived teLEC exert mitogenic effect on tumor cells, in the primary tumor. • teLEC act as fibroblast-like cells in the tumor microenvironment. • It warrants to revisit the “vascular-centric view” of LECs.
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- 2020
8. Contralateral Vascularized Lymph Node Transfer: An Optimized Mouse Model
- Author
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Jean-Luc Nizet, Silvia Blacher, Tania Durré, Giulia Virginia Vottero, Alain Plenevaux, Florent Morfoisse, Guillaume Becker, Agnès Noël, and Mohamed Ali Bahri
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Pathology ,medicine.medical_specialty ,vascularized lymph node transfer ,business.industry ,mouse model ,lcsh:Surgery ,lcsh:RD1-811 ,lymphedema ,medicine.disease ,medicine.anatomical_structure ,Lymphedema ,Medicine ,business ,Lymph node - Abstract
Background Vascularized lymph node transfer (VLNT) is one of the surgical options in the treatment of lymphedema, but its mechanism of action has not yet been firmly clarified. In the VLNT mouse models described so far, the lymph node flap is performed between two different sites in the same lymphedematous paw. In this study, we describe an optimized VLNT mouse model using the contralateral paw as donor site, thus removing the bias of transferring a lymph node already damaged by irradiation and/or surgery required to induce lymphedema. Methods A lymphedema was induced on the left posterior paw in four experimental groups of mice (n = 8). Two weeks later, group 1 was the sham one, group 2 underwent a VLNT from the right inguinal region to the left, in group 3 a vascular endothelial growth factor (VEGF)-C sponge was placed alone in the left inguinal region, and in group 4 a VEGF-C sponge was associated to the VLNT. The 32 mice were followed during 3 months. Outcomes included paws volume, skin quality, inflammation in the lymphedematous tissue, and lymphatic network density and function. Results Group 4 displayed significantly higher (p Conclusions This optimized mouse model of VLNT shows to be handy and effective. It could be exploited to perform further experimental studies about the influence of VLNT on lymphedema. Moreover, the local association between VLNT and biological compounds in this model allows it to be a good preclinical model to identify new potential drugs in lymphedema.
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- 2019
9. Ear Sponge Assay: A Method to Investigate Angiogenesis and Lymphangiogenesis in Mice
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Maureen, Van de Velde, Melissa, García-Caballero, Tania, Durré, Frédéric, Kridelka, and Agnès, Noël
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Neovascularization, Pathologic ,Endothelial Cells ,Ear ,Gelatin Sponge, Absorbable ,Mice ,Imaging, Three-Dimensional ,Microscopy, Fluorescence ,Cell Line, Tumor ,Culture Media, Conditioned ,Animals ,Biological Assay ,Female ,Lymphangiogenesis ,Peptide Hydrolases - Abstract
Angiogenesis and lymphangiogenesis have become important research areas in the biomedical field. The outgrowth of new blood (angiogenesis) and lymphatic (lymphangiogenesis) vessels from preexisting ones is involved in many pathologies including cancer. In-depth investigations of molecular determinants such as proteases in these complex processes require reliable in vivo models. Here we present the ear sponge assay as an easy, rapid, quantitative and reproducible model of angiogenesis and lymphangiogenesis. In this system, a gelatin sponge soaked with tumor cells, cell-conditioned medium, or a compound to be tested is implanted, for 2-4 weeks, between the two mouse ear skin layers. The two vascular networks are next examined through histological procedures.
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- 2018
10. Ear Sponge Assay: A Method to Investigate Angiogenesis and Lymphangiogenesis in Mice
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Agnès Noël, Frédéric Kridelka, Melissa García-Caballero, Tania Durré, and Maureen Van de Velde
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0301 basic medicine ,Proteases ,Pathology ,medicine.medical_specialty ,Angiogenesis ,Cancer ,Biology ,medicine.disease ,biology.organism_classification ,Lymphangiogenesis ,03 medical and health sciences ,Important research ,Sponge ,030104 developmental biology ,Lymphatic system ,In vivo ,medicine - Abstract
Angiogenesis and lymphangiogenesis have become important research areas in the biomedical field. The outgrowth of new blood (angiogenesis) and lymphatic (lymphangiogenesis) vessels from preexisting ones is involved in many pathologies including cancer. In-depth investigations of molecular determinants such as proteases in these complex processes require reliable in vivo models. Here we present the ear sponge assay as an easy, rapid, quantitative and reproducible model of angiogenesis and lymphangiogenesis. In this system, a gelatin sponge soaked with tumor cells, cell-conditioned medium, or a compound to be tested is implanted, for 2-4 weeks, between the two mouse ear skin layers. The two vascular networks are next examined through histological procedures.
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- 2018
11. Modeling pre-metastatic lymphvascular niche in the mouse ear sponge assay
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Silvia Blacher, Tania Durré, Agnès Noël, Charlotte Erpicum, Frédéric Kridelka, Cédric Balsat, Maureen Van de Velde, Melissa García-Caballero, and Vincent Lambert
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0301 basic medicine ,Pathology ,medicine.medical_specialty ,Injections, Intradermal ,Niche ,Melanoma, Experimental ,Biology ,Models, Biological ,Article ,03 medical and health sciences ,0302 clinical medicine ,Implants, Experimental ,In vivo ,Lymphatic Spread ,Lymphatic vessel ,medicine ,Image Processing, Computer-Assisted ,Animals ,Cell Proliferation ,Lymphatic Vessels ,Multidisciplinary ,Cell growth ,Anatomy ,Sciences bio-médicales et agricoles ,Lymphangiogenesis ,Mice, Inbred C57BL ,030104 developmental biology ,medicine.anatomical_structure ,Lymphatic system ,030220 oncology & carcinogenesis ,Lymphatic Metastasis ,Gelatin ,Biological Assay ,Lymph ,Lymph Nodes - Abstract
Lymphangiogenesis, the formation of new lymphatic vessels, occurs in primary tumors and in draining lymph nodes leading to pre-metastatic niche formation. Reliable in vivo models are becoming instrumental for investigating alterations occurring in lymph nodes before tumor cell arrival. In this study, we demonstrate that B16F10 melanoma cell encapsulation in a biomaterial, and implantation in the mouse ear, prevents their rapid lymphatic spread observed when cells are directly injected in the ear. Vascular remodeling in lymph nodes was detected two weeks after sponge implantation, while their colonization by tumor cells occurred two weeks later. In this model, a huge lymphangiogenic response was induced in primary tumors and in pre-metastatic and metastatic lymph nodes. In control lymph nodes, lymphatic vessels were confined to the cortex. In contrast, an enlargement and expansion of lymphatic vessels towards paracortical and medullar areas occurred in pre-metastatic lymph nodes. We designed an original computerized-assisted quantification method to examine the lymphatic vessel structure and the spatial distribution. This new reliable and accurate model is suitable for in vivo studies of lymphangiogenesis, holds promise for unraveling the mechanisms underlying lymphatic metastases and pre-metastatic niche formation in lymph nodes, and will provide new tools for drug testing., info:eu-repo/semantics/published
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- 2017
12. Mesenchymal Stem Cells Shed Amphiregulin at the Surface of Lung Carcinoma Cells in a Juxtacrine Manner
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Silvia Blacher, Irina Primac, Benoît Detry, Anne Masset, Ludovic Maertens, Oriane Carnet, Agnès Noël, Didier Cataldo, Tania Durré, Christel Pequeux, Jean-Michel Foidart, Guy Jerusalem, Jenny Paupert, Christine Gilles, and Julie Lecomte
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Cancer Research ,Pathology ,medicine.medical_specialty ,Stromal cell ,Bone Marrow Cells ,Cell Communication ,ADAM Proteins -- antagonists & inhibitors -- metabolism ,Biology ,ADAM17 Protein ,Amphiregulin ,lcsh:RC254-282 ,Cell Membrane -- metabolism ,Article ,Carcinoma, Lewis Lung -- pathology ,Carcinoma, Lewis Lung ,Mesenchymal Stem Cells -- metabolism ,Mice ,Spheroids, Cellular ,Amphiregulin -- metabolism ,medicine ,Fluorescence Resonance Energy Transfer ,Image Processing, Computer-Assisted ,Tumor Cells, Cultured ,Animals ,Neoplasm Invasiveness ,Cell Communication -- physiology ,Neoplasm Metastasis ,Bone Marrow Cells -- metabolism ,Cell Proliferation ,Cell Membrane ,Mesenchymal stem cell ,Lewis lung carcinoma ,Mesenchymal Stem Cells ,Sciences bio-médicales et agricoles ,lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,Juxtacrine signalling ,Mice, Inbred C57BL ,ADAM Proteins ,Neoplasm Invasiveness -- pathology ,medicine.anatomical_structure ,Tumor progression ,Cancer cell ,Cancer research ,Female ,Bone marrow ,Neoplasm Metastasis -- pathology ,Neoplasm Transplantation - Abstract
Solid tumors comprise cancer cells and different supportive stromal cells, including mesenchymal stem cells (MSCs), which have recently been shown to enhance tumor growth and metastasis. We provide new mechanistic insights into how bone marrow (BM)-derived MSCs co-injected with Lewis lung carcinoma cells promote tumor growth and metastasis in mice. The proinvasive effect of BM-MSCs exerted on tumor cells relies on an unprecedented juxtacrine action of BM-MSC, leading to the trans-shedding of amphiregulin (AREG) from the tumor cell membrane by tumor necrosis factor-α-converting enzyme carried by the BM-MSC plasma membrane. The released soluble AREG activates cancer cells and promotes their invasiveness. This novel concept is supported by the exploitation of different 2D and 3D culture systems and by pharmacological approaches using a tumor necrosis factor-α-converting enzyme inhibitor and AREG-blocking antibodies. Altogether, we here assign a new function to BM-MSC in tumor progression and establish an uncovered link between AREG and BM-MSC., info:eu-repo/semantics/published
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- View/download PDF
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