534 results on '"Pizzinat A"'
Search Results
2. Correction: IPSC derived cardiac fibroblasts of DMD patients show compromised actin microfilaments, metabolic shift and pro-fibrotic phenotype
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Soussi, Salwa, Savchenko, Lesia, Rovina, Davide, Iacovoni, Jason S., Gottinger, Andrea, Vialettes, Maxime, Pioner, Josè-Manuel, Farini, Andrea, Mallia, Sara, Rabino, Martina, Pompilio, Giulio, Parini, Angelo, Lairez, Olivier, Gowran, Aoife, and Pizzinat, Nathalie
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- 2023
- Full Text
- View/download PDF
3. IPSC derived cardiac fibroblasts of DMD patients show compromised actin microfilaments, metabolic shift and pro-fibrotic phenotype
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Soussi, Salwa, Savchenko, Lesia, Rovina, Davide, Iacovoni, Jason S., Gottinger, Andrea, Vialettes, Maxime, Pioner, Josè-Manuel, Farini, Andrea, Mallia, Sara, Rabino, Martina, Pompilio, Giulio, Parini, Angelo, Lairez, Olivier, Gowran, Aoife, and Pizzinat, Nathalie
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- 2023
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- View/download PDF
4. Engineered and Mimicked Extracellular Nanovesicles for Therapeutic Delivery
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Verena Poinsot, Nathalie Pizzinat, and Varravaddheay Ong-Meang
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extracellular vesicles ,exosomes ,hybrid exosome ,exosome-mime ,drug delivery ,Chemistry ,QD1-999 - Abstract
Exosomes are spherical extracellular nanovesicles with an endosomal origin and unilamellar lipid-bilayer structure with sizes ranging from 30 to 100 nm. They contain a large range of proteins, lipids, and nucleic acid species, depending on the state and origin of the extracellular vesicle (EV)-secreting cell. EVs’ function is to encapsulate part of the EV-producing cell content, to transport it through biological fluids to a targeted recipient, and to deliver their cargos specifically within the aimed recipient cells. Therefore, exosomes are considered to be potential biological drug-delivery systems that can stably deliver their cargo into targeted cells. Various cell-derived exosomes are produced for medical issues, but their use for therapeutic purposes still faces several problems. Some of these difficulties can be avoided by resorting to hemisynthetic approaches. We highlight here the uses of alternative exosome-mimes involving cell-membrane coatings on artificial nanocarriers or the hybridization between exosomes and liposomes. We also detail the drug-loading strategies deployed to make them drug-carrier systems and summarize the ongoing clinical trials involving exosomes or exosome-like structures. Finally, we summarize the open questions before considering exosome-like disposals for confident therapeutic delivery.
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- 2024
- Full Text
- View/download PDF
5. Galanin Coordinates Macrophage-Associated Fibro-Inflammatory Response and Mitochondrial Integrity in Myocardial Infarction Reperfusion Injury
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Savchenko, Lesia, primary, Kramar, Solomiia, additional, Todua, Nika, additional, Marsal, Dimitri, additional, Kang, Ryeonshi, additional, Swiader, Audrey, additional, Pizzinat, Nathalie, additional, and Kunduzova, Oksana, additional
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- 2024
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6. Cardiac macrophage subsets differentially regulate lymphatic network remodeling during pressure overload
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Mathilde Bizou, Romain Itier, Mina Majdoubi, Dounia Abbadi, Estelle Pichery, Marianne Dutaur, Dimitri Marsal, Denis Calise, Barbara Garmy-Susini, Victorine Douin-Echinard, Jérome Roncalli, Angelo Parini, and Nathalie Pizzinat
- Subjects
Medicine ,Science - Abstract
Abstract The lymphatic network of mammalian heart is an important regulator of interstitial fluid compartment and immune cell trafficking. We observed a remodeling of the cardiac lymphatic vessels and a reduced lymphatic efficiency during heart hypertrophy and failure induced by transverse aortic constriction. The lymphatic endothelial cell number of the failing hearts was positively correlated with cardiac function and with a subset of cardiac macrophages. This macrophage population distinguished by LYVE-1 (Lymphatic vessel endothelial hyaluronic acid receptor-1) and by resident macrophage gene expression signature, appeared not replenished by CCR2 mediated monocyte infiltration during pressure overload. Isolation of macrophage subpopulations showed that the LYVE-1 positive subset sustained in vitro and in vivo lymphangiogenesis through the expression of pro-lymphangiogenic factors. In contrast, the LYVE-1 negative macrophage subset strongly expressed MMP12 and decreased the endothelial LYVE-1 receptors in lymphatic endothelial cells, a feature of cardiac lymphatic remodeling in failing hearts. The treatment of mice with a CCR2 antagonist during pressure overload modified the proportion of macrophage subsets within the pathological heart and preserved lymphatic network from remodeling. This study reports unknown and differential functions of macrophage subpopulations in the regulation of cardiac lymphatic during pathological hypertrophy and may constitute a key mechanism underlying the progression of heart failure.
- Published
- 2021
- Full Text
- View/download PDF
7. Extracellular vesicles of MSCs and cardiomyoblasts are vehicles for lipid mediators
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Pizzinat, Nathalie, Ong-Meang, Varravaddheay, Bourgailh-Tortosa, Florence, Blanzat, Muriel, Perquis, Lucie, Cussac, Daniel, Parini, Angelo, and Poinsot, Verena
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- 2020
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8. Kidney inflammaging is promoted by CCR2+ macrophages and tissue-derived micro-environmental factors
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Lefèvre, Lise, Iacovoni, Jason S., Martini, Hélène, Bellière, Julie, Maggiorani, Damien, Dutaur, Marianne, Marsal, Dimitri J., Decaunes, Pauline, Pizzinat, Nathalie, Mialet-Perez, Jeanne, Cussac, Daniel, Parini, Angelo, and Douin-Echinard, Victorine
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- 2021
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9. Engineered and Mimicked Extracellular Nanovesicles for Therapeutic Delivery.
- Author
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Poinsot, Verena, Pizzinat, Nathalie, and Ong-Meang, Varravaddheay
- Subjects
EXTRACELLULAR vesicles ,BIOLOGICAL systems ,EXOSOMES ,LIPOSOMES ,OPEN-ended questions - Abstract
Exosomes are spherical extracellular nanovesicles with an endosomal origin and unilamellar lipid-bilayer structure with sizes ranging from 30 to 100 nm. They contain a large range of proteins, lipids, and nucleic acid species, depending on the state and origin of the extracellular vesicle (EV)-secreting cell. EVs' function is to encapsulate part of the EV-producing cell content, to transport it through biological fluids to a targeted recipient, and to deliver their cargos specifically within the aimed recipient cells. Therefore, exosomes are considered to be potential biological drug-delivery systems that can stably deliver their cargo into targeted cells. Various cell-derived exosomes are produced for medical issues, but their use for therapeutic purposes still faces several problems. Some of these difficulties can be avoided by resorting to hemisynthetic approaches. We highlight here the uses of alternative exosome-mimes involving cell-membrane coatings on artificial nanocarriers or the hybridization between exosomes and liposomes. We also detail the drug-loading strategies deployed to make them drug-carrier systems and summarize the ongoing clinical trials involving exosomes or exosome-like structures. Finally, we summarize the open questions before considering exosome-like disposals for confident therapeutic delivery. [ABSTRACT FROM AUTHOR]
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- 2024
- Full Text
- View/download PDF
10. Lymphatic and Immune Cell Cross-Talk Regulates Cardiac Recovery After Experimental Myocardial Infarction
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Houssari, Mahmoud, Dumesnil, Anais, Tardif, Virginie, Kivelä, Riikka, Pizzinat, Nathalie, Boukhalfa, Ines, Godefroy, David, Schapman, Damien, Hemanthakumar, Karthik A., Bizou, Mathilde, Henry, Jean-Paul, Renet, Sylvanie, Riou, Gaetan, Rondeaux, Julie, Anouar, Youssef, Adriouch, Sahil, Fraineau, Sylvain, Alitalo, Kari, Richard, Vincent, Mulder, Paul, and Brakenhielm, Ebba
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- 2020
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11. Metabolic, Apoptotic and Fibro-Inflammatory Profiles of the Heart Exposed to Environmental Electromagnetic Fields
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Savchenko, Lesia, primary, Martinelli, Ilenia, additional, Marsal, Dimitri, additional, Batkivska, Oksana, additional, Zhdan, Vyacheslav, additional, Kaidashev, Igor, additional, Pizzinat, Nathalie, additional, Boal, Frederic, additional, Tronchere, Helene, additional, Tao, Junwu, additional, and Kunduzova, Oksana, additional
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- 2023
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- View/download PDF
12. A complete fronthaul CWDM single fiber solution including improved monitoring scheme.
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Thierno Diallo, Bertrand Le Guyader, Anna Pizzinat, Stéphane Gosselin, Philippe Chanclou, Fabienne Saliou, Amr Abdelfattath, and Christelle Aupetit-Berthelemot
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- 2015
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13. Age-Related Shift in Cardiac and Metabolic Phenotyping Linked to Inflammatory Cytokines and Antioxidant Status in Mice.
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Kang, Ryeonshi, Laborde, Charlotte, Savchenko, Lesia, Swiader, Audrey, Pizzinat, Nathalie, Marsal, Dimitri, Sainte-Marie, Yannis, Boal, Frederic, Tronchere, Helene, Roncalli, Jerome, and Kunduzova, Oksana
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OXIDANT status ,MICE ,CYTOKINES ,OXIDATIVE stress ,RESISTIN ,INTERLEUKIN-6 ,GLUTATHIONE - Abstract
Age-related alterations in cardiac function, metabolic, inflammatory and antioxidant profiles are associated with an increased risk of cardiovascular mortality and morbidity. Here, we examined cardiac and metabolic phenotypes in relation to inflammatory status and antioxidant capacity in young, middle-aged and old mice. Real-time reverse transcription–polymerase chain reactions were performed on myocardium and immunoassays on plasma. Left ventricular (LV) structure and function were assessed by echocardiography using high-frequency ultrasound. Middle-aged mice exhibited an altered metabolic profile and antioxidant capacity compared to young mice, whereas myocardial expression of inflammatory factors (TNFα, IL1β, IL6 and IL10) remained unchanged. In contrast, old mice exhibited increased expression of inflammatory cytokines and plasma levels of resistin compared to young and middle-aged mice (p < 0.05). The pro-inflammatory signature of aged hearts was associated with alterations in glutathione redox homeostasis and elevated contents of 4-hydroxynonenal (4-HNE), a marker of lipid peroxidation and oxidative stress. Furthermore, echocardiographic parameters of LV systolic and diastolic functions were significantly altered in old mice compared to young mice. Taken together, these findings suggest age-related shifts in cardiac phenotype encompass the spectrum of metabo-inflammatory abnormalities and altered redox homeostasis. [ABSTRACT FROM AUTHOR]
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- 2023
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14. Extracellular Vesicles Produced by the Cardiac Microenvironment Carry Functional Enzymes to Produce Lipid Mediators In Situ
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Ong-Meang, Varravaddheay, primary, Blanzat, Muriel, additional, Savchenko, Lesia, additional, Perquis, Lucie, additional, Guardia, Mégane, additional, Pizzinat, Nathalie, additional, and Poinsot, Verena, additional
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- 2023
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15. WDM PONs based on colorless technology
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Saliou, Fabienne, Simon, Gael, Chanclou, Philippe, Pizzinat, Anna, Lin, Huafeng, Zhou, Enyu, and Xu, Zhiguang
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- 2015
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16. Optical fiber solution for mobile fronthaul to achieve cloud radio access network.
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Philippe Chanclou, Anna Pizzinat, Fabien Le Clech, To-Linh Reedeker, Yannick Lagadec, Fabienne Saliou, Bertrand Le Guyader, Laurent Guillo, Qian Deniel, Stéphane Gosselin, Sy Dat Le, Thierno Diallo, Romain Brenot, Francois Lelarge, Lucia Marazzi, Paola Parolari, Mario Martinelli, Sean O'Duill, Simon Arega Gebrewold, David Hillerkuss, Juerg Leuthold, Giancarlo Gavioli, and Paola Galli
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- 2013
17. Digital radio over fiber for LTE-advanced: Opportunities and challenges.
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Ahmed Saadani, Mamdouh El Tabach, Anna Pizzinat, Michel Nahas, Pascal Pagnoux, Serban Purge, and Yu Bao
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- 2013
18. Fixed and Mobile Convergence: Which role for optical networks?
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Stéphane Gosselin, Anna Pizzinat, Xavier Grall, Dirk Breuer, Eckard Bogenfeld, Jose Alfonso Torrijos Gijon, Ali Hamidian, and Neiva Fonseca
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- 2015
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19. Future Internet in Home Area Networks: Towards Optical Solutions?
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Roberto Gaudino, Daniel Cardenas, Martial Bellec, Benoît Charbonnier, Noëlla Evanno, Philippe Guignard, Sylvain Meyer, Anna Pizzinat, Ingo Möllers, and Dieter Jäger
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- 2009
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20. Ultra Wide Band over fibre transparent architecture for High Bit-rate Home Networks
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Pizzinat, Anna, Payoux, Franck, Charbonnier, Benoit, Meyer, Sylvain, Al Agha, Khaldoun, editor, Carcelle, Xavier, editor, and Pujolle, Guy, editor
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- 2008
- Full Text
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21. Jitter impact on mobile fronthaul links.
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Thierno A. Diallo, Anna Pizzinat, Philippe Chanclou, Fabienne Saliou, F. Deletre, and Christelle Aupetit-Berthelemot
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- 2014
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22. Things you should know about fronthaul.
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Anna Pizzinat, Philippe Chanclou, Thierno Diallo, and Fabienne Saliou
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- 2014
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23. An energy consumption comparison of different mobile backhaul and fronthaul optical access architectures.
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Nicola Carapellese, Anna Pizzinat, Massimo Tornatore, Philippe Chanclou, and Stéphane Gosselin
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- 2014
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24. Low-PMD spun fibers
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Galtarossa, Andrea, Griggio, Paola, Palmieri, Luca, Pizzinat, Anna, Bjarklev, Anders, editor, Chowdhury, Dipak, editor, Nakasawa, Masataka, editor, Weber, Hans-Georg, editor, Someda, Carlo G., editor, Galtarossa, Andrea, editor, and Menyuk, Curtis R., editor
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- 2005
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25. Cardiac macrophage subsets differentially regulate lymphatic network remodeling during pressure overload
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Estelle Pichery, Mathilde Bizou, Angelo Parini, Mina Majdoubi, Barbara Garmy-Susini, Jerome Roncalli, Romain Itier, Dounia Abbadi, Nathalie Pizzinat, Victorine Douin-Echinard, Dimitri Marsal, Marianne Dutaur, Denis Calise, Institut de médecine moléculaire de Rangueil (I2MR), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées- Institut Fédératif de Recherche Bio-médicale Institution (IFR150)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), Institut Cardiomet [CHU Toulouse], Pôle Cardiovasculaire et Métabolique [CHU Toulouse], Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), UMS006, pizzinat, Nathalie, Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-IFR150-Institut National de la Santé et de la Recherche Médicale (INSERM), Hôpital de Rangueil, CHU Toulouse [Toulouse], and Institut CARDIOMET - CHU Toulouse
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Male ,Pathology ,[SDV]Life Sciences [q-bio] ,Vesicular Transport Proteins ,030204 cardiovascular system & hematology ,Monocytes ,Electrocardiography ,0302 clinical medicine ,Macrophage ,Medicine ,Lymphangiogenesis ,0303 health sciences ,Multidisciplinary ,Cell Polarity ,Endothelial stem cell ,[SDV] Life Sciences [q-bio] ,Lymphatic Endothelium ,Lymphatic system ,medicine.anatomical_structure ,medicine.medical_specialty ,Receptors, CCR2 ,Science ,government.form_of_government ,Cardiology ,CHO Cells ,Article ,03 medical and health sciences ,Cricetulus ,Interstitial fluid ,Pressure ,Lymphatic vessel ,Animals ,Humans ,Spiro Compounds ,RNA, Messenger ,Lymphatic Vessels ,030304 developmental biology ,Pressure overload ,business.industry ,Macrophages ,Myocardium ,Endothelial Cells ,Cardiovascular biology ,Benzoxazines ,Mice, Inbred C57BL ,Gene Expression Regulation ,government ,Transcriptome ,business - Abstract
The lymphatic network of mammalian heart is an important regulator of interstitial fluid compartment and immune cell trafficking. We observed a remodeling of the cardiac lymphatic vessels and a reduced lymphatic efficiency during heart hypertrophy and failure induced by transverse aortic constriction. The lymphatic endothelial cell number of the failing hearts was positively correlated with cardiac function and with a subset of cardiac macrophages. This macrophage population distinguished by LYVE-1 (Lymphatic vessel endothelial hyaluronic acid receptor-1) and by resident macrophage gene expression signature, appeared not replenished by CCR2 mediated monocyte infiltration during pressure overload. Isolation of macrophage subpopulations showed that the LYVE-1 positive subset sustained in vitro and in vivo lymphangiogenesis through the expression of pro-lymphangiogenic factors. In contrast, the LYVE-1 negative macrophage subset strongly expressed MMP12 and decreased the endothelial LYVE-1 receptors in lymphatic endothelial cells, a feature of cardiac lymphatic remodeling in failing hearts. The treatment of mice with a CCR2 antagonist during pressure overload modified the proportion of macrophage subsets within the pathological heart and preserved lymphatic network from remodeling. This study reports unknown and differential functions of macrophage subpopulations in the regulation of cardiac lymphatic during pathological hypertrophy and may constitute a key mechanism underlying the progression of heart failure.
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- 2021
- Full Text
- View/download PDF
26. France Telecom's PON deployment, learnt lessons and next steps.
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Philippe Chanclou, Bruno Capelle, Benoît Charbonnier, Jean-Luc Courant, Y. Denis, Naveena Genay, Stéphane Gosselin, Dominique Kurz, B. Landousies, E. Le Bris, Bertrand Le Guyader, Anna Pizzinat, and Fabienne Saliou
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- 2013
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27. WDM-FDM approach for a multiservice home network.
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Joffray Guillory, K. Chikha, Anna Pizzinat, Philippe Guignard, Benoît Charbonnier, J. Etrillard, and Catherine Algani
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- 2013
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28. Local production of tenascin-C acts as a trigger for monocyte/macrophage recruitment that provokes cardiac dysfunction
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Abbadi, Dounia, Laroumanie, Fanny, Bizou, Mathilde, Pozzo, Joffrey, Daviaud, Danièle, Delage, Christine, Calise, Denis, Gaits-Iacovoni, Fréderique, Dutaur, Marianne, Tortosa, Florence, Renaud-Gabardos, Edith, Douin-Echinard, Victorine, Prats, Anne-Catherine, Roncalli, Jerome, Parini, Angelo, and Pizzinat, Nathalie
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- 2018
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29. N × N Coupler Uniformity in a CWDM Passive Star Home Network Based on Multimode Fiber: A Time-Effective Calculation Method.
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F. Richard, Philippe Guignard, Anna Pizzinat, Eric Tanguy, and H. W. Li
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- 2012
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30. Metformin Attenuates Postinfarction Myocardial Fibrosis and Inflammation in Mice
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Halyna Loi, Solomiia Kramar, Charlotte Laborde, Dimitri Marsal, Nathalie Pizzinat, Daniel Cussac, Jerome Roncalli, Frederic Boal, Helene Tronchere, Oleksandra Oleshchuk, Mykhaylo Korda, Oksana Kunduzova, I.Horbachevsky Ternopil State Medical University, Ternopil, Ukraine, Institut des Maladies Métaboliques et Casdiovasculaires (UPS/Inserm U1297 - I2MC), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées, and pizzinat, Nathalie
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Male ,Ventricular Remodeling ,QH301-705.5 ,Myocardium ,[SDV]Life Sciences [q-bio] ,fibrosis ,Article ,Mice, Inbred C57BL ,[SDV] Life Sciences [q-bio] ,Chemistry ,Mice ,myocardial infarction ,inflammation ,Animals ,Hypoglycemic Agents ,Biology (General) ,cardiac remodeling ,metformin ,QD1-999 - Abstract
International audience; Diabetes is a major risk factor for the development of cardiovascular disease with a higher incidence of myocardial infarction. This study explores the role of metformin, a first-line antihyperglycemic agent, in postinfarction fibrotic and inflammatory remodeling in mice. Three-month-old C57BI/6J mice were submitted to 30 min cardiac ischemia followed by reperfusion for 14 days. Intraperitoneal treatment with metformin (5 mg/kg) was initiated 15 min after the onset of reperfusion and maintained for 14 days. Real-time PCR was used to determine the levels of COL3A1, αSMA, CD68, TNF-α and IL-6. Increased collagen deposition and infiltration of macrophages in heart tissues are associated with upregulation of the inflammation-associated genes in mice after 14 days of reperfusion. Metformin treatment markedly reduced postinfarction fibrotic remodeling and CD68-positive cell population in mice. Moreover, metformin resulted in reduced expression of COL3A1, αSMA and CD68 after 14 days of reperfusion. Taken together, these results open new perspectives for the use of metformin as a drug that counteracts adverse myocardial fibroticand inflammatory remodeling after MI.
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- 2021
- Full Text
- View/download PDF
31. Radio-Over-Fiber Architectures.
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Joffray Guillory, Sylvain Meyer, Isbelle Sianud, Anne-Marie Ulmer-Moll, Benoît Charbonnier, Anna Pizzinat, and Catherine Algani
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- 2010
- Full Text
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32. Perspective in next-generation home networks: Toward optical solutions?
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Roberto Gaudino, Daniel Cardenas, Martial Bellec, Benoît Charbonnier, Noëlla Evanno, Philippe Guignard, Sylvain Meyer, Anna Pizzinat, Ingo Möllers, and Dieter Jäger
- Published
- 2010
- Full Text
- View/download PDF
33. Extracellular Vesicles Produced by the Cardiac Microenvironment Carry Functional Enzymes to Produce Lipid Mediators In Situ
- Author
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Varravaddheay Ong-Meang, Muriel Blanzat, Lesia Savchenko, Lucie Perquis, Mégane Guardia, Nathalie Pizzinat, Verena Poinsot, Interactions moléculaires et réactivité chimique et photochimique (IMRCP), Institut de Chimie de Toulouse (ICT), Institut de Recherche pour le Développement (IRD)-Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS)-Institut National Polytechnique (Toulouse) (Toulouse INP), Université de Toulouse (UT)-Institut de Recherche pour le Développement (IRD)-Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Institut Ecologie et Environnement (INEE), Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS)-Fédération de Recherche Fluides, Energie, Réacteurs, Matériaux et Transferts (FERMAT), Institut National des Sciences Appliquées - Toulouse (INSA Toulouse), Institut National des Sciences Appliquées (INSA)-Université de Toulouse (UT)-Institut National des Sciences Appliquées (INSA)-Université de Toulouse (UT)-Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Centre National de la Recherche Scientifique (CNRS)-Institut National Polytechnique (Toulouse) (Toulouse INP), Université de Toulouse (UT)-Institut National des Sciences Appliquées - Toulouse (INSA Toulouse), Institut National des Sciences Appliquées (INSA)-Université de Toulouse (UT)-Institut National des Sciences Appliquées (INSA)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), SMODD - Systèmes Moléculaires Organisés et Développement Durable (SMODD), Institut National des Sciences Appliquées (INSA)-Université de Toulouse (UT)-Institut National des Sciences Appliquées (INSA)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS)-Institut de Chimie de Toulouse (ICT), Research and Legal Issues Kyiv International University, BIBAC - Chimie analytique et interactions biomolécules - matière molle biomimétique (BIBAC), Institut de médecine moléculaire de Rangueil (I2MR), Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Université de Toulouse (UT)- Institut Fédératif de Recherche Bio-médicale Institution (IFR150)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), and Université de Toulouse (UT)
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Inorganic Chemistry ,Organic Chemistry ,[CHIM]Chemical Sciences ,General Medicine ,Physical and Theoretical Chemistry ,Molecular Biology ,Spectroscopy ,Catalysis ,Computer Science Applications - Abstract
International audience; The impact of the polyunsaturated fatty acids (PUFAs) at physiological concentrations on the composition of eicosanoids transported within the extracellular vesicles (EVs) of rat bone marrow mesenchymal stem cells and cardiomyoblasts was reported by our group in 2020. The aim of this article was to extend this observation to cells from the cardiac microenvironment involved in the processes of inflammation, namely mouse J774 macrophages and rat heart mesenchymal stem cells cMSCs. Moreover, to enhance our capacity to understand the paracrine exchange between these orchestrators of cardiac inflammation, we investigated some machinery involved in the eicosanoid’s synthesis transported by the EVs produced by these cells (including the two formerly described cells: bone marrow mesenchymal stem cells BM-MSC and cardiomyoblasts H9c2). We analyzed the oxylipin and the enzymatic content of the EVs collected from cell cultures supplemented (or not) with PUFAs. We prove that large eicosanoid profiles are exported in the EVs by the cardiac microenvironment cells, but also that these EVs carry some critical and functional biosynthetic enzymes, allowing them to synthesize inflammation bioactive compounds by sensing their environment. Moreover, we demonstrate that these are functional. This observation reinforces the hypothesis that EVs are key factors in paracrine signaling, even in the absence of the parent cell. We also reveal a macrophage-specific behavior, as we observed a radical change in the lipid mediator profile when small EVs derived from J774 cells were exposed to PUFAs. To summarize, we prove that the EVs, due to the carried functional enzymes, can alone produce bioactive compounds, in the absence of the parent cell, by sensing their environment. This makes them potential circulating monitoring entities.
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- 2023
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34. Ultra wideband over fibre transparent architecture for high-bit-rate home networks.
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Anna Pizzinat, Franck Payoux, Benoît Charbonnier, and Sylvain Meyer
- Published
- 2008
- Full Text
- View/download PDF
35. Selective Cardiomyocyte Oxidative Stress Leads to Bystander Senescence of Cardiac Stromal Cells
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Martini, Hélène, Lefevre, Lise, Sayir, Sylvain, Itier, Romain, Maggiorani, Damien, Dutaur, Marianne, Marsal, Dimitri, Roncalli, Jérôme, Pizzinat, Nathalie, Cussac, Daniel, Parini, Angelo, Mialet-Perez, Jeanne, Douin-Echinard, Victorine, Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM), pizzinat, Nathalie, Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Toulouse III - Paul Sabatier (UT3), and Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées
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Male ,Aging ,CCR2+ Macrophages ,[SDV]Life Sciences [q-bio] ,Mice, Transgenic ,cardiac mesenchymal stromal cells ,SASP ,Article ,lcsh:Chemistry ,Mice ,Animals ,oxidative stress ,Myocytes, Cardiac ,Monoamine Oxidase ,lcsh:QH301-705.5 ,Cells, Cultured ,Cellular Senescence ,Bystander Effect ,Mice, Inbred C57BL ,[SDV] Life Sciences [q-bio] ,lcsh:Biology (General) ,lcsh:QD1-999 ,stress-induced premature senescence ,monoamine oxidase A ,Stromal Cells ,DNA Damage - Abstract
International audience; Accumulation of senescent cells in tissues during normal or accelerated aging has been shown to be detrimental and to favor the outcomes of age-related diseases such as heart failure (HF). We have previously shown that oxidative stress dependent on monoamine oxidase A (MAOA) activity in cardiomyocytes promotes mitochondrial damage, the formation of telomere-associated foci, senescence markers, and triggers systolic cardiac dysfunction in a model of transgenic mice overexpressing MAOA in cardiomyocytes (Tg MAOA). However, the impact of cardiomyocyte oxidative stress on the cardiac microenvironment in vivo is still unclear. Our results showed that systolic cardiac dysfunction in Tg MAOA mice was strongly correlated with oxidative stress induced premature senescence of cardiac stromal cells favoring the recruitment of CCR2+ monocytes and the installation of cardiac inflammation. Understanding the interplay between oxidative stress induced premature senescence and accelerated cardiac dysfunction will help to define new molecular pathways at the crossroad between cardiac dysfunction and accelerated aging, which could contribute to the increased susceptibility of the elderly to HF.
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- 2021
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36. Retrospective Study of 573 Patients with Heart Failure Evaluated for Coronary Artery Disease at Toulouse University Center, France
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Antoine Deney, Vanessa Nader, Anthony Matta, Romain Itier, Pauline Fournier, Olivier Lairez, Nathalie Pizzinat, Didier Carrié, Frédéric Boal, Michel Galinier, Oksana Kunduzova, Rania Azar, and Jerome Roncalli
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Male ,Heart Failure ,Heart Failure, Diastolic ,Age Factors ,Stroke Volume ,General Medicine ,Coronary Artery Disease ,Coronary Angiography ,Sex Factors ,Heart Disease Risk Factors ,Risk Factors ,Clinical Research ,Humans ,Female ,France ,Angioplasty, Balloon, Coronary ,Aged ,Heart Failure, Systolic ,Retrospective Studies - Abstract
BACKGROUND Heart failure (HF) most commonly occurs due to ischemic heart disease from stenotic coronary artery disease (CAD). HF is classified into 3 groups based on the percentage of the ejection fraction (EF): reduced (HFrEF), mid-range (HFmrEF), and preserved (HFpEF). This retrospective study included 573 patients who presented with HF based on the evaluation of EF and were evaluated for CAD by coronary angiography before undergoing coronary angioplasty at a single center in Toulouse, France. MATERIAL AND METHODS This retrospective observational study included patients recently diagnosed with HF or acute decompensation of chronic HF and referred for coronary angiography at Toulouse University Hospital between January 2019 and May 2020. RESULTS Significant CAD was found in 55.8%, 55%, and 55% of the whole population, HFpEF, and HFrEF groups, respectively. Older age, male sex, and diabetes mellitus were the main risk factors for ischemic HF. Except for age and sex, patients with ischemic HFpEF were comparable to those with non-ischemic HFpEF, unlike the ischemic HFrEF group, which had more common cardiovascular risk factors than the non-ischemic HFrEF group. The ischemic HFpEF group had an older age and higher rate of dyslipidemia than the ischemic HFrEF group. CONCLUSIONS At our center, CAD was diagnosed in more than half of patients who presented with heart failure with preserved or reduced EF. Older age and male sex were the common risk factors in patients with HFpEF and HFrEF.
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- 2022
37. Retrospective Study of 573 Patients with Heart Failure Evaluated for Coronary Artery Disease at Toulouse University Center, France
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Deney, Antoine, primary, Nader, Vanessa, additional, Matta, Anthony, additional, Itier, Romain, additional, Fournier, Pauline, additional, Lairez, Olivier, additional, Pizzinat, Nathalie, additional, Carrié, Didier, additional, Boal, Frédéric, additional, Galinier, Michel, additional, Kunduzova, Oksana, additional, Azar, Rania, additional, and Roncalli, Jerome, additional
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- 2021
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38. Platelet derived serotonin drives the activation of rat cardiac fibroblasts by 5-HT2A receptors
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Yabanoglu, Samiye, Akkiki, Mansour, Seguelas, Marie-Helène, Mialet-Perez, Jeanne, Parini, Angelo, and Pizzinat, Nathalie
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- 2009
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39. Genetic deletion of MAO-A promotes serotonin-dependent ventricular hypertrophy by pressure overload
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Lairez, Olivier, Calise, Denis, Bianchi, Pascale, Ordener, Catherine, Spreux-Varoquaux, Odile, Guilbeau-Frugier, Céline, Escourrou, Ghislaine, Seif, Isabelle, Roncalli, Jérôme, Pizzinat, Nathalie, Galinier, Michel, Parini, Angelo, and Mialet-Perez, Jeanne
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- 2009
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40. Metformin Attenuates Postinfarction Myocardial Fibrosis and Inflammation in Mice
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Loi, Halyna, primary, Kramar, Solomiia, additional, Laborde, Charlotte, additional, Marsal, Dimitri, additional, Pizzinat, Nathalie, additional, Cussac, Daniel, additional, Roncalli, Jerome, additional, Boal, Frederic, additional, Tronchere, Helene, additional, Oleshchuk, Oleksandra, additional, Korda, Mykhaylo, additional, and Kunduzova, Oksana, additional
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- 2021
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41. Cardiac macrophage subsets differentially regulate lymphatic network remodeling during pressure overload
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Bizou, Mathilde, primary, Itier, Romain, additional, Majdoubi, Mina, additional, Abbadi, Dounia, additional, Pichery, Estelle, additional, Dutaur, Marianne, additional, Marsal, Dimitri, additional, Calise, Denis, additional, Garmy-Susini, Barbara, additional, Douin-Echinard, Victorine, additional, Roncalli, Jérome, additional, Parini, Angelo, additional, and Pizzinat, Nathalie, additional
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- 2021
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42. Incidence of ‘Candidatus Liberibacter europaeus’ and phytoplasmas in Cacopsylla species (Hemiptera: Psyllidae) and their host/shelter plants
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Camerota, Caterina, Raddadi, Noura, Pizzinat, Alan, Gonella, Elena, Crotti, Elena, Tedeschi, Rosemarie, Mozes-Daube, Netta, Ember, Ibolya, Acs, Zoltan, Kolber, Maria, Zchori-Fein, Einat, Daffonchio, Daniele, and Alma, Alberto
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- 2012
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43. Access network evolution: optical fibre to the subscribers and impact on the metropolitan and home networks
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Chanclou, P., Belfqih, Z., Charbonnier, B., Duong, T., Frank, F., Genay, N., Huchard, M., Guignard, P., Guillo, L., Landousies, B., Pizzinat, A., Ramanitra, H., Saliou, F., Durel, S., Urvoas, P., Ouzzif, M., and Le Masson, J.
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- 2008
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44. Platelet activation and arterial peripheral serotonin turnover in cardiac remodeling associated to aortic stenosis
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Rouzaud-Laborde, Charlotte, Delmas, Clément, Pizzinat, Nathalie, Tortosa, Florence, Garcia, Cédric, Mialet-Perez, Jeanne, Payrastre, Bernard, Sié, Pierre, Spreux-Varoquaux, Odile, Sallerin, Brigitte, Carrié, Didier, Galinier, Michel, Parini, Angelo, and Lairez, Olivier
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- 2015
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45. Les EVs des MSCs et cardiomyoblastes sont des véhicules pour les médiateurs lipidiques
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Angelo Parini, Florence Bourgailh-Tortosa, Lucie Perquis, Muriel Blanzat, Nathalie Pizzinat, Varravaddheay Ong-Meang, Daniel Cussac, Verena Poinsot, Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées, Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées, Interactions moléculaires et réactivité chimique et photochimique (IMRCP), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)-Institut de Chimie du CNRS (INC)-Institut de Chimie de Toulouse (ICT-FR 2599), Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Institut de Chimie du CNRS (INC)-Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Toulouse (UT), Institut de Chimie de Toulouse (ICT), Institut de Recherche pour le Développement (IRD)-Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS)-Institut National Polytechnique (Toulouse) (Toulouse INP), Université de Toulouse (UT)-Institut de Recherche pour le Développement (IRD)-Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Institut Ecologie et Environnement (INEE), Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS)-Fédération de Recherche Fluides, Energie, Réacteurs, Matériaux et Transferts (FERMAT), Institut National des Sciences Appliquées - Toulouse (INSA Toulouse), Institut National des Sciences Appliquées (INSA)-Université de Toulouse (UT)-Institut National des Sciences Appliquées (INSA)-Université de Toulouse (UT)-Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Centre National de la Recherche Scientifique (CNRS)-Institut National Polytechnique (Toulouse) (Toulouse INP), Université de Toulouse (UT)-Institut National des Sciences Appliquées - Toulouse (INSA Toulouse), Institut National des Sciences Appliquées (INSA)-Université de Toulouse (UT)-Institut National des Sciences Appliquées (INSA)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), SMODD - Systèmes Moléculaires Organisés et Développement Durable (SMODD), Institut National des Sciences Appliquées (INSA)-Université de Toulouse (UT)-Institut National des Sciences Appliquées (INSA)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS)-Institut de Chimie de Toulouse (ICT), BIBAC - Chimie analytique et interactions biomolécules - matière molle biomimétique (BIBAC), pizzinat, Nathalie, and Institut National de la Santé et de la Recherche Médicale (INSERM)
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0301 basic medicine ,Cell signaling ,[SDV.BC]Life Sciences [q-bio]/Cellular Biology ,Biochemistry ,Cell Line ,03 medical and health sciences ,chemistry.chemical_compound ,Bone Marrow ,Animals ,Humans ,[SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology ,Oxylipins ,Progenitor cell ,[SDV.BC] Life Sciences [q-bio]/Cellular Biology ,ComputingMilieux_MISCELLANEOUS ,Inflammation ,030102 biochemistry & molecular biology ,Mesenchymal stem cell ,Mesenchymal Stem Cells ,Heart ,General Medicine ,Lipid signaling ,Extracellular vesicles ,Lipid Metabolism ,Eicosapentaenoic acid ,Microvesicles ,Rats ,Cell biology ,030104 developmental biology ,chemistry ,Docosahexaenoic acid ,Lipid mediator ,Eicosanoids ,Arachidonic acid ,lipids (amino acids, peptides, and proteins) ,Inflammation Mediators ,Myoblasts, Cardiac ,PUFA - Abstract
International audience; Recent works reported the relevance of cellular exosomes in the evolution of different pathologies. However, most of these studies focused on the ability of exosomes to convey mi-RNA from cell to cell. The level of knowledge concerning the transport of lipid mediators by these nanovesicles is more than fragmented. The role of lipid mediators in the inflammatory signaling is fairly well described, in particular concerning the derivatives of the arachidonic acid (AA), called eicosanoïds or lipid mediators. The aim of the present work was to study the transport of these lipids within the extracellular vesicles of rat bone marrow mesenchymal stem cells (BM-MSC) and the cardiomyoblast cell line H9c2. We were able to characterize, for the first time, complete profiles of oxilipins within these nanovesicles. We studied also the impact on these profiles, of the polyunsaturated fatty acids (PUFAs) know to be precursors of the inflammatory signaling molecules (AA, eicosapentaenoic acid EPA and Docosahexaenoic acid DHA), at physiological concentrations. By growing the progenitor cells under PUFAs supplementation, we provide a comprehensive assessment of the beneficial effect of u-3 PUFA therapy. Actually, our results tend to support the resolving role of the inflammation that stromal cell-derived extracellular vesicles can have within the cardiac microenvironment.
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- 2020
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46. Dose-dependent activation of distinct hypertrophic pathways by serotonin in cardiac cells
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Villeneuve, C., Caudrillier, A., Ordener, C., Pizzinat, N., Parini, A., and Mialet-Perez, J.
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Heart cells -- Physiological aspects ,Heart cells -- Research ,Heart enlargement -- Care and treatment ,Heart enlargement -- Research ,Monoamine oxidase -- Physiological aspects ,Monoamine oxidase -- Research ,Serotonin -- Physiological aspects ,Serotonin -- Research ,Biological sciences - Abstract
There is substantial evidence supporting a hypertrophic action of serotonin [5-hydroxytryptamine (5-HT)] in cardiomyocytes. However, little is known about the mechanisms involved. We previously demonstrated that 5-HT-induced hypertrophy depends, in part, on the generation of reactive oxygen species by monoamine oxidase-A (MAO-A) (see Ref. 3). Cardiomyocytes express 5-HT2 receptors, which may also participate in hypertrophy. Here, we analyzed the respective contribution of 5-[HT.sub.2] receptors and MAO-A in H9C2 cardiomyoblast hypertrophy. 5-HT induced a dose-dependent increase in [sup.3]H]leucine incorporation and stimulation of two markers of cardiac hypertrophy, ANF-luc and [alpha]SK-actin-luc reporter genes. Experiments using 1 [micro]M 5-HT showed that hypertrophic response occurred independently from MAO-A. Using pharmacological inhibitors (M 100907 and ketanserin), we identified a novel mechanism of action involving 5-[HT.sub.2A] receptors and requiring [Ca.sup.2+]/calcineurin/nuclear factor of activated T-cell activation. The activation of this hypertrophic pathway was fully prevented by 5-[HT.sub.2A] inhibitors and was unaffected by MAO inhibition. When 10 [micro]M 5-HT was used, an additional hypertrophic response, prevented by the MAO inhibitors pargyline and RO 41-1049, was observed. Unlike the 5-[HT.sub.2A]receptor-mediated H9C2 cell hypertrophy, MAO-A-dependent hypertrophic response required activation of extracellular-regulated kinases. In conclusion, our results show the existence of a dose-dependent shift of activation of distinct intracellular pathways involved in 5-HT-mediated hypertrophy of cardiac cells. 5-hydroxytryptamine; 5-hydroxytryptamine 2A; monoamine oxidase type A; hypertrophy
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- 2009
47. Aging induces cardiac mesenchymal stromal cell senescence and promotes endothelial cell fate of the CD90 + subset
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Martini, Hélène, Iacovoni, Jason, Maggiorani, Damien, Dutaur, Marianne, Marsal, Dimitri, Roncalli, Jerome, Itier, Romain, Dambrin, Camille, Pizzinat, Nathalie, Mialet‐Perez, Jeanne, Cussac, Daniel, Parini, Angelo, Lefèvre, Lise, Douin‐Echinard, Victorine, Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM), Fédération hospitalo-universitaire Innovative Medicine for the Prevention and treAtment of Cardiovascular and meTabolic diseases [CHU Toulouse] (FHU IMPACT), Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), Université Fédérale Toulouse Midi-Pyrénées, Conseil Régional Midi‐Pyrénées, Grant/Award Number: APRTCN MiPy 2013 and APRTT MiPy 2011, Institut National de la Santé et de la Recherche Médicale, Fédération Française de Cardiologie., pizzinat, Nathalie, Fédération hospitalo-universitaire 'Innovative Medicine for the Prevention and treAtment of Cardiovascular and meTabolic diseases' [CHU Toulouse] (FHU IMPACT), and Institut CARDIOMET - CHU Toulouse
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Aging ,senescence ,[SDV]Life Sciences [q-bio] ,Interleukin-1beta ,heart ,[SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC] ,[SDV.BC.IC] Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB] ,Mice ,[SDV.BC.IC]Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB] ,[SDV.BC.BC] Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC] ,Animals ,Humans ,IL-1ß ,Cellular Senescence ,Original Paper ,Myocardium ,Endothelial Cells ,Cell Differentiation ,Mesenchymal Stem Cells ,Interferon-beta ,Original Papers ,macrophages ,CD90 ,[SDV] Life Sciences [q-bio] ,Thy-1 Antigens ,mesenchymal stromal cells ,IL‐1ß - Abstract
International audience; Aging is a major risk factor in the development of chronic diseases, especially cardiovascular diseases. Age-related organ dysfunction is strongly associated with the accumulation of senescent cells. Cardiac mesenchymal stromal cells (cMSCs), deemed part of the microenvironment, modulate cardiac homeostasis through their vascular differentiation potential and paracrine activity. Transcriptomic analysis of cMSCs identified age-dependent biological pathways regulating immune responses and angiogenesis. Aged cMSCs displayed a senescence program characterized by Cdkn2a expression, decreased proliferation and clonogenicity, and acquisition of a senescence-associated secretory phenotype (SASP). Increased CCR2-dependent monocyte recruitment by aged cMSCs was associated with increased IL-1ß production by inflammatory macrophages in the aging heart. In turn, IL-1ß induced senescence in cMSCs and mimicked age-related phenotypic changes such as decreased CD90 expression. The CD90+ and CD90- cMSC subsets had biased vascular differentiation potentials, and CD90+ cMSCs were more prone to acquire markers of the endothelial lineage with aging. These features were related to the emergence of a new cMSC subset in the aging heart, expressing CD31 and endothelial genes. These results demonstrate that cMSC senescence and SASP production are supported by the installation of an inflammatory amplification loop, which could sustain cMSC senescence and interfere with their vascular differentiation potentials.
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- 2019
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48. Kidney inflammaging is promoted by CCR2
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Lise, Lefèvre, Jason S, Iacovoni, Hélène, Martini, Julie, Bellière, Damien, Maggiorani, Marianne, Dutaur, Dimitri J, Marsal, Pauline, Decaunes, Nathalie, Pizzinat, Jeanne, Mialet-Perez, Daniel, Cussac, Angelo, Parini, and Victorine, Douin-Echinard
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Inflammation ,Male ,Aging ,Receptors, CCR2 ,Macrophages ,CX3C Chemokine Receptor 1 ,Mesenchymal stromal cells ,Kidney ,Senescence ,Inflammaging ,Monocytes ,Mice, Inbred C57BL ,Mice ,Cellular Microenvironment ,CD73 ,Animals ,Cytokines ,CCR2 ,Original Article ,Cellular Senescence - Abstract
The incidence of disorders associated with low inflammatory state, such as chronic kidney disease, increases in the elderly. The accumulation of senescent cells during aging and the senescence-associated secretory phenotype, which leads to inflammaging, is known to be deleterious and account for progressive organ dysfunction. To date, the cellular actors implicated in chronic inflammation in the kidney during aging are still not well characterized. Using the DECyt method, based on hierarchical clustering of flow cytometry data, we showed that aging was associated with significant changes in stromal cell diversity in the kidney. In particular, we identified two cell populations up-regulated with aging, the mesenchymal stromal cell subset (kMSC) expressing CD73 and the monocyte-derived Ly6C+ CCR2+ macrophage subset expressing pro-inflammatory cytokines. Aged CD73+ kMSCs depicted senescence associated features with low proliferation rate, increased DNA damage foci and Ccl2 expression. Using co-cultures experiments, we showed that aged CD73+ kMSC promoted monocyte activation and secretion of inflammatory cytokines albeit less efficiently than young CD73+ kMSCs. In the context of ageing, increased frequency of CD73+ kMSC subpopulations could provide additional niche factors to newly recruited monocytes favoring a positive regulatory loop in response to local inflammation. Interfering with such partnership during aging could be a valuable approach to regulate kidney inflammaging and to limit the risk of developing chronic kidney disease in the elderly. Supplementary Information The online version contains supplementary material available at 10.1007/s00018-020-03719-0.
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- 2020
49. Lymphatic and Immune Cell Cross-Talk Regulates Cardiac Recovery After Experimental Myocardial Infarction
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Anaïs Dumesnil, Sylvanie Renet, Sylvain Fraineau, Nathalie Pizzinat, Kari Alitalo, Jean-Paul Henry, Mahmoud Houssari, David Godefroy, Sahil Adriouch, Youssef Anouar, Ebba Brakenhielm, Paul Mulder, Riikka Kivelä, Vincent Richard, Damien Schapman, Karthik Amudhala Hemanthakumar, Gaëtan Riou, Inès Boukhalfa, Julie Rondeaux, Virginie Tardif, Mathilde Bizou, Institut National de la Santé et de la Recherche Médicale (INSERM), Endothélium, valvulopathies et insuffisance cardiaque (EnVI), Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Normandie Université (NU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Wihuri Research Institute [Helsinki, Finland], Institut des Maladies Métaboliques et Casdiovasculaires (UPS/Inserm U1297 - I2MC), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM), Différenciation et communication neuronale et neuroendocrine (DC2N), Plate-Forme de Recherche en Imagerie Cellulaire de Haute-Normandie (PRIMACEN), Normandie Université (NU)-Normandie Université (NU)-Institute for Research and Innovation in Biomedicine (IRIB), Normandie Université (NU)-Normandie Université (NU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-High-tech Research Infrastructures for Life Sciences (HeRacLeS), Normandie Université (NU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Physiopathologie, Autoimmunité, maladies Neuromusculaires et THErapies Régénératrices (PANTHER), Lebon, Alexis, Kivelä Lab, Faculty of Medicine, Research Programs Unit, University of Helsinki, CAN-PRO - Translational Cancer Medicine Program, HUSLAB, Translational Cancer Biology (TCB) Research Programme, and Kari Alitalo / Principal Investigator
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CD4-Positive T-Lymphocytes ,Male ,STIMULATION ,Time Factors ,[SDV]Life Sciences [q-bio] ,Vascular Endothelial Growth Factor C ,Cell ,Myocardial Infarction ,heart failure ,VEGF-C ,CD8-Positive T-Lymphocytes ,030204 cardiovascular system & hematology ,Ventricular Function, Left ,ACTIVATION ,0302 clinical medicine ,VESSELS ,Interferon ,Myocardial infarction ,ComputingMilieux_MISCELLANEOUS ,0303 health sciences ,interferon ,Dependovirus ,macrophages ,[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system ,3. Good health ,Lymphangiogenesis ,lymphangiogenesis ,Lymphatic system ,medicine.anatomical_structure ,Female ,medicine.symptom ,Cardiology and Cardiovascular Medicine ,Signal Transduction ,medicine.drug ,Genetic Vectors ,Inflammation ,DENDRITIC CELLS ,Interferon-gamma ,03 medical and health sciences ,Immune system ,[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system ,medicine ,Animals ,Rats, Wistar ,Lymphatic Vessels ,030304 developmental biology ,REPAIR ,business.industry ,Myocardium ,INFLAMMATORY RESPONSE ,Genetic Therapy ,Recovery of Function ,Vascular Endothelial Growth Factor Receptor-3 ,medicine.disease ,Mice, Inbred C57BL ,Disease Models, Animal ,inflammation ,3121 General medicine, internal medicine and other clinical medicine ,Heart failure ,Immunology ,T-CELLS ,3111 Biomedicine ,business - Abstract
Objective: Lymphatics play an essential pathophysiological role in promoting fluid and immune cell tissue clearance. Conversely, immune cells may influence lymphatic function and remodeling. Recently, cardiac lymphangiogenesis has been proposed as a therapeutic target to prevent heart failure after myocardial infarction (MI). We investigated the effects of gene therapy to modulate cardiac lymphangiogenesis post-MI in rodents. Second, we determined the impact of cardiac-infiltrating T cells on lymphatic remodeling in the heart. Approach and Results: Comparing adenoviral versus adeno-associated viral gene delivery in mice, we found that only sustained VEGF (vascular endothelial growth factor)-C C156S therapy, achieved by adeno-associated viral vectors, increased cardiac lymphangiogenesis, and led to reduced cardiac inflammation and dysfunction by 3 weeks post-MI. Conversely, inhibition of VEGF-C/-D signaling, through adeno-associated viral delivery of soluble VEGFR3 (vascular endothelial growth factor receptor 3), limited infarct lymphangiogenesis. Unexpectedly, this treatment improved cardiac function post-MI in both mice and rats, linked to reduced infarct thinning due to acute suppression of T-cell infiltration. Finally, using pharmacological, genetic, and antibody-mediated prevention of cardiac T-cell recruitment in mice, we discovered that both CD4 + and CD8 + T cells potently suppress, in part through interferon-γ, cardiac lymphangiogenesis post-MI. Conclusions: We show that resolution of cardiac inflammation after MI may be accelerated by therapeutic lymphangiogenesis based on adeno-associated viral gene delivery of VEGF-C C156S . Conversely, our work uncovers a major negative role of cardiac-recruited T cells on lymphatic remodeling. Our results give new insight into the interconnection between immune cells and lymphatics in orchestration of cardiac repair after injury.
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- 2020
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50. Role of endothelial AADC in cardiac synthesis of serotonin and nitrates accumulation.
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Charlotte Rouzaud-Laborde, Naïma Hanoun, Ipek Baysal, Jean-Simon Rech, Céline Mias, Denis Calise, Pierre Sicard, Céline Frugier, Marie-Helène Seguelas, Angelo Parini, and Nathalie Pizzinat
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Medicine ,Science - Abstract
Serotonin (5-HT) regulates different cardiac functions by acting directly on cardiomyocytes, fibroblasts and endothelial cells. Today, it is widely accepted that activated platelets represent a major source of 5-HT. In contrast, a supposed production of 5-HT in the heart is still controversial. To address this issue, we investigated the expression and localization of 5-HT synthesizing enzyme tryptophan hydroxylase (TPH) and L-aromatic amino acid decarboxylase (AADC) in the heart. We also evaluated their involvement in cardiac production of 5-HT. TPH1 was weakly expressed in mouse and rat heart and appeared restricted to mast cells. Degranulation of mast cells by compound 48/80 did not modify 5-HT cardiac content in mice. Western blots and immunolabelling experiments showed an abundant expression of AADC in the mouse and rat heart and its co-localization with endothelial cells. Incubation of cardiac homogenate with the AADC substrate (5-hydroxy-L-tryptophan) 5-HTP or intraperitoneal injection of 5-HTP in mice significantly increased cardiac 5-HT. These effects were prevented by the AADC inhibitor benserazide. Finally, 5-HTP administration in mice increased phosphorylation of aortic nitric oxide synthase 3 at Ser (1177) as well as accumulation of nitrates in cardiac tissue. This suggests that the increase in 5-HT production by AADC leads to activation of endothelial and cardiac nitric oxide pathway. These data show that endothelial AADC plays an important role in cardiac synthesis of 5-HT and possibly in 5-HT-dependent regulation of nitric oxide generation.
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- 2012
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