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101. Desmin is a modifier of dystrophic muscle features in Mdx mice

Author

Ferry, Arnaud, primary, Messéant, Julien, additional, Parlakian, Ara, additional, Lemaitre, Mégane, additional, Roy, Pauline, additional, Delacroix, Clément, additional, Lilienbaum, Alain, additional, Hovhannisyan, Yeranuhi, additional, Furling, Denis, additional, Klein, Arnaud, additional, Li, Zhenlin, additional, and Agbulut, Onnik, additional

Published
2019
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104. Dynamic expression of synemin isoforms in mouse embryonic stem cells and neural derivatives

Author

de Souza Martins Sheila C, Agbulut Onnik, Diguet Nicolas, Larcher Jean-Christophe, Paulsen Bruna S, Rehen Stevens K, Moura-Neto Vivaldo, Paulin Denise, Li Zhenlin, and Xue Zhigang

Subjects
Cytology, QH573-671
Abstract

Abstract Background Intermediate filaments (IFs) are major components of the mammalian cytoskeleton and expressed in cell-type-specific patterns. Morphological changes during cell differentiation are linked to IF network remodeling. However, little is known concerning the presence and the role of IFs in embryonic stem (ES) cells and during their differentiation. Results We have examined the expression profile of synemin isoforms in mouse pluripotent ES cells and during their neural differentiation induced by retinoic acid. Using RT-PCR, Western blotting and immunostaining, we show that synemin M is present at both mRNA and protein levels in undifferentiated ES cells as early as pluripotency factor Oct-3/4 and IF keratin 8. Synemin H was produced only in neural precursors when neural differentiation started, concurrently with synemin M, nestin and glial fibrillary acidic protein. However, both synemin H and M were restricted to the progenitor line during the neural differentiation program. Our in vivo analysis also confirmed the expression of synemins H/M in multipotent neural stem cells in the subventricular zone of the adult brain, a neurogenic germinal niche of the mice. Knocking down synemin in ES cells by shRNA lentiviral particles transduction has no influence on expression of Oct4, Nanog and SOX2, but decreased keratin 8 expression. Conclusions Our study shows a developmental stage specific regulation of synemin isoforms in ES cells and its neural derivatives. These findings represent the first evidence that synemins could potentially be useful markers for distinguishing multipotent ES cells from undifferentiated neural stem cells and more committed progenitor cells.

Published
2011
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106. MiRroring the Multiple Potentials of MicroRNAs in Acute Myocardial Infarction

Author

Paiva, Solenne and Agbulut, Onnik

Subjects
lcsh:Diseases of the circulatory (Cardiovascular) system, lcsh:RC666-701, cardiac biomarkers, cardiomyocytes maturation, acute myocardial infarction, regenerative medicine, Review, Cardiovascular Medicine, Cardiology and Cardiovascular Medicine, microRNAs
Abstract

At present, cardiovascular diseases are depicted to be the leading cause of death worldwide according to the World Health Organization. In the future, projections predict that ischemic heart disease will persist in the top main causes of illness. Within this alarming context, some tiny master regulators of gene expression programs, namely, microRNAs (miRNAs) carry three promising potentials. In fact, miRNAs can prove to be useful not only in terms of biomarkers allowing heart injury detection but also in terms of therapeutics to overcome limitations of past strategies and treat the lesions. In a more creative approach, they can even be used in the area of human engineered cardiac tissues as maturation tools for cardiomyocytes (CMs) derived from pluripotent stem cell. Very promising not only for patient-specific cell-based therapies but also to develop biomimetic microsystems for disease modeling and drug screening, these cells greatly contribute to personalized medicine. To get into the heart of the matter, the focus of this review lies primarily on miRNAs as acute myocardial infarction (AMI) biomarkers. Only large cohort studies comprising over 100 individuals to reach a potent statistical value were considered. Certain miRNAs appeared to possibly complement protein-based biomarkers and classical risk factors. Some were even described to bear potential in the discrimination of similar symptomatic pathologies. However, differences between pre-analytical and analytical approaches substantially influenced miRNA data. Further supported by meta-analysis studies, this problem had to be addressed. A detailed critical analysis of each step to define miRNAs biomarker potential is provided to inspire a future improved universal strategy. Interestingly, a recurrent set of cardiomyocyte-enriched miRNAs was found, namely, miR-1; miR-133; miR-208a/b; and miR-499a. Each member of this myomiRs group displayed promising roles either individually or in combination as AMI diagnostic or prognostic biomarkers. Furthermore, a precise combo was shown to be powerful enough to transdifferentiate human fibroblasts into CMs opening doors in the therapeutics. Following these discoveries, they also emerged as optional tools to transfect in order to mature CMs derived from pluripotent stem cells. Ultimately, the multiple potentials carried by the myomiRs miR-1; miR-133; miR-208a/b; and miR-499a still remain to be fully unveiled.

Published
2017

107. Distinct Fiber Type Signature in Mouse Muscles Expressing a Mutant Lamin A Responsible for Congenital Muscular Dystrophy in a Patient

Author

Barateau, Alice, Vadrot, Nathalie, Agbulut, Onnik, Vicart, Patrick, Batonnet-Pichon, Sabrina, Buendia, Brigitte, Unité de Biologie Fonctionnelle et Adaptative (BFA (UMR_8251 / U1133)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Diderot - Paris 7 (UPD7), Cellules Souches et Biothérapies (CSB), Adaptation Biologique et Vieillissement = Biological Adaptation and Ageing (B2A), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-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)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-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), Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-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)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), and Université Pierre et Marie Curie - Paris 6 (UPMC)-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)

Subjects
congenital, hereditary, and neonatal diseases and abnormalities, congenital muscular dystrophy, muscle fiber type transition, lcsh:Biology (General), integumentary system, [SDV]Life Sciences [q-bio], embryonic structures, myosin heavy chain IIA, lcsh:QH301-705.5, Article, lamin A
Abstract

International audience; Specific mutations in LMNA, which encodes nuclear intermediate filament proteins lamins A/C, affect skeletal muscle tissues. Early-onset LMNA myopathies reveal different alterations of muscle fibers, including fiber type disproportion or prominent dystrophic and/or inflammatory changes. Recently, we identified the p.R388P LMNA mutation as responsible for congenital muscular dystrophy (L-CMD) and lipodystrophy. Here, we asked whether viral-mediated expression of mutant lamin A in murine skeletal muscles would be a pertinent model to reveal specific muscle alterations. We found that the total amount and size of muscle fibers as well as the extent of either inflammation or muscle regeneration were similar to wildtype or mutant lamin A. In contrast, the amount of fast oxidative muscle fibers containing myosin heavy chain IIA was lower upon expression of mutant lamin A, in correlation with lower expression of genes encoding transcription factors MEF2C and MyoD. These data validate this in vivo model for highlighting distinct muscle phenotypes associated with different lamin contexts. Additionally, the data suggest that alteration of muscle fiber type identity may contribute to the mechanisms underlying physiopathology of L-CMD related to R388P mutant lamin A.

Published
2017

108. Voluntary Exercise Improves Cardiac Function and Prevents Cardiac Remodeling in a Mouse Model of Dilated Cardiomyopathy

Author

Deloux, Robin, Vitiello, Damien, Mougenot, Nathalie, Noirez, Philippe, Li, Zhenlin, Mericskay, Mathias, Ferry, Arnaud, Agbulut, Onnik, Signalisation et physiopathologie cardiovasculaire (UMRS1180), Institut National de la Santé et de la Recherche Médicale (INSERM), Adaptation Biologique et Vieillissement = Biological Adaptation and Ageing (B2A), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Institut de Biologie Paris Seine (IBPS), Sorbonne Université (SU)-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), Université Sorbonne Paris Cité (USPC), Institut de recherche biomédicale et d’épidémiologie du sport (IRMES - URP_7329), Institut national du sport, de l'expertise et de la performance (INSEP)-Université de Paris (UP), Phénotypage du petit animal (UMS28), Sorbonne Université (SU), Institut de Myologie, Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Association française contre les myopathies (AFM-Téléthon)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Institut national du sport, de l'expertise et de la performance (INSEP)-Université Paris Cité (UPCité), Centre de recherche en Myologie – U974 SU-INSERM, Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Université Paris Cité (UPCité), Quaireau, Valérie, Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-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), and Centre National de la Recherche Scientifique (CNRS)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Association française contre les myopathies (AFM-Téléthon)-Sorbonne Université (SU)

Subjects
non-ischemic cardiac disease, dilated cardiomyopathy, non-forced exercise, [SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, [SDV.MHEP.PHY] Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO], Physiology, wheel exercise, [SDV.MHEP.PHY]Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO], [SHS.SPORT.PS]Humanities and Social Sciences/Sport/Sport physiology, [SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, Original Research
Abstract

International audience; Objective: Despite the indubitable beneficial effect of exercise to prevent of cardiovascular diseases, there is still a lack of studies investigating the impact of exercise in non-ischemic dilated cardiomyopathy. Here, we investigated the impact of voluntary exercise on cardiac function in a mouse model of non-ischemic dilated cardiomyopathy (αMHC-MerCreMer:Sf/Sf), induced by cardiac-specific inactivation of the Serum Response Factor.Materials and Methods: Seven days after tamoxifen injection, 20 αMHC-MerCreMer:Sf/Sf mice were assigned to sedentary (n = 8) and exercise (n = 12) groups. Seven additional αMHC-MerCreMer:Sf/Sf mice without tamoxifen injection were used as control. The exercise group performed 4 weeks of voluntary running on wheel (1.8 ± 0.12 km/day). Cardiac function, myocardial fibrosis, and mitochondrial energetic pathways were then blindly assessed.Results: Exercised mice exhibited a smaller decrease of left ventricular (LV) fractional shortening and ejection fraction compared to control mice. This was associated with a lower degree of LV remodeling in exercised mice, as shown by a lower LV end-systolic intrerventricular septal and posterior wall thickness decrease from baseline values compared to sedentary mice. Moreover, exercised mice displayed a reduced gene expression of atrial and brain natriuretic factors. These benefits were associated by a reduced level of myocardial fibrosis. In addition, exercised mice exhibited a higher mitochondrial aconitase, voltage-dependent anion-selective channel 1 and PPAR gamma coactivators-1 alpha proteins levels suggesting that the increase of mitochondrial biogenesis and/or metabolism slowed the progression of dilated cardiomyopathy in exercised animals.Conclusions: In conclusion, our results support the role of voluntary exercise to improve outcomes in non-ischemic dilated heart failure (HF) and also support its potential for a routine clinical use in the future.

Published
2017

111. Lipin1 deficiency causes sarcoplasmic reticulum stress and chaperone‐responsive myopathy

Author

Rashid, Talha, primary, Nemazanyy, Ivan, additional, Paolini, Cecilia, additional, Tatsuta, Takashi, additional, Crespin, Paul, additional, Villeneuve, Delphine, additional, Brodesser, Susanne, additional, Benit, Paule, additional, Rustin, Pierre, additional, Baraibar, Martin A, additional, Agbulut, Onnik, additional, Olivier, Anne, additional, Protasi, Feliciano, additional, Langer, Thomas, additional, Chrast, Roman, additional, Lonlay, Pascale, additional, Foucauld, Helene, additional, Blaauw, Bert, additional, and Pende, Mario, additional

Published
2018
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112. Acellular therapeutic approach for heart failure: in vitro production of extracellular vesicles from human cardiovascular progenitors

Author

El Harane, Nadia, primary, Kervadec, Anaïs, additional, Bellamy, Valérie, additional, Pidial, Laetitia, additional, Neametalla, Hany J, additional, Perier, Marie-Cécile, additional, Lima Correa, Bruna, additional, Thiébault, Léa, additional, Cagnard, Nicolas, additional, Duché, Angéline, additional, Brunaud, Camille, additional, Lemitre, Mathilde, additional, Gauthier, Jeanne, additional, Bourdillon, Alexandra T, additional, Renault, Marc P, additional, Hovhannisyan, Yeranuhi, additional, Paiva, Solenne, additional, Colas, Alexandre R, additional, Agbulut, Onnik, additional, Hagège, Albert, additional, Silvestre, Jean-Sébastien, additional, Menasché, Philippe, additional, and Renault, Nisa K E, additional

Published
2018
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116. Design of Functional Electrospun Scaffolds Based on Poly(glycerol sebacate) Elastomer and Poly(lactic acid) for Cardiac Tissue Engineering

Author

Flaig, Florence, Ragot, Hélène, Simon, Alexandre, Revet, Gaëlle, Kitsara, Maria, Kitasato, Lisa, Hébraud, Anne, Agbulut, Onnik, and Schlatter, Guy

Abstract

Many works focus on the use of polyesters such as poly(lactic acid) (PLA) to produce nanofibrous scaffolds for cardiac tissue engineering. However, such scaffolds are hydrophobic and difficult to functionalize. Here, we show that adding 30% of poly(glycerol sebacate) (PGS) elastomer within PLA leads to PLA:PGS scaffolds with improved biological properties, depending on the processing parameters. Two categories of fibers were produced by blend electrospinning, with diameters of 600 and 1300 nm. The resulting fibers were cured at 90 or 120 °C to achieve two different cross-linking densities. The designed scaffolds were considered for cytocompatibility, biocompatibility, biodegradability, and chemical and mechanical properties. Our results demonstrated that the presence of PGS increases the hydrophilicity of the material and thus improves surface functionalization by Matrigel or laminin coating, commonly used cell culture matrices. PLA:PGS scaffolds associated with Matrigel or laminin allow an increased material–cell interaction. Moreover, the cardiomyocytes seeded on such scaffolds acquire a morphology similar to that observed in native tissue, the result being more remarkable on fibers having the smallest diameter and the highest PGS cross-linking density. In addition, these scaffolds induce neovascularization without an inflammatory response and foreign body giant cell response after grafting on a mouse heart. Hence, the improved biocompatibility and the ability to support cardiomyocyte development suggest that thin

Published
2024
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117. Dystrophin restoration therapy improves both the reduced excitability and the force drop induced by lengthening contractions in dystrophic mdx skeletal muscle

Author

Roy, Pauline, Rau, Fredérique, Ochala, Julien, Messéant, Julien, Fraysse, Bodvael, Lainé, Jeanne, Agbulut, Onnik, Butler-Browne, Gillian, Furling, Denis, Ferry, Arnaud, Roy, Pauline, Rau, Fredérique, Ochala, Julien, Messéant, Julien, Fraysse, Bodvael, Lainé, Jeanne, Agbulut, Onnik, Butler-Browne, Gillian, Furling, Denis, and Ferry, Arnaud

Abstract

Background: The greater susceptibility to contraction-induced skeletal muscle injury (fragility) is an important dystrophic feature and tool for testing preclinic dystrophin-based therapies for Duchenne muscular dystrophy. However, how these therapies reduce the muscle fragility is not clear. Methods: To address this question, we first determined the event(s) of the excitation-contraction cycle which is/are altered following lengthening (eccentric) contractions in the mdx muscle. Results: We found that the immediate force drop following lengthening contractions, a widely used measure of muscle fragility, was associated with reduced muscle excitability. Moreover, the force drop can be mimicked by an experimental reduction in muscle excitation of uninjured muscle. Furthermore, the force drop was not related to major neuromuscular transmission failure, excitation-contraction uncoupling, and myofibrillar impairment. Secondly, and importantly, the re-expression of functional truncated dystrophin in the muscle of mdx mice using an exon skipping strategy partially prevented the reductions in both force drop and muscle excitability following lengthening contractions. Conclusion: We demonstrated for the first time that (i) the increased susceptibility to contraction-induced muscle injury in mdx mice is mainly attributable to reduced muscle excitability; (ii) dystrophin-based therapy improves fragility of the dystrophic skeletal muscle by preventing reduction in muscle excitability.

Published
2016

118. Myostatin is a key mediator between energy metabolism and\ud endurance capacity of skeletal muscle

Author

Mouisel, Etienne, Relizani, Karima, Mille-Hamard, Laurence, Denis, Raphael, Hourde, Christophe, Agbulut, Onnik, Patel, Ketan, Arandel, Ludovic, Morales-Gonzalez, Susanne, Vignaud, Alban, Garcia, Luis, Ferry, Arnaud, Luquet, Serge, Billat, Veronique, Ventura-Clapier, Renee, Schuelke, Markus, and Amthor, Helge

Subjects
musculoskeletal system
Abstract

Myostatin (Mstn) participates in the regulation of skeletal muscle size and has emerged as a regulator of muscle metabolism. Here, we hypothesized that lack of myostatin profoundly depresses oxidative phosphorylation-dependent muscle function. Toward this end, we explored Mstn/ mice as a model for the constitutive absence of myostatin and AAV-mediated overexpression of myostatin propeptide as a model of myostatin blockade in adult wild-type mice. We show that muscles from Mstn/ mice, although larger and stronger, fatigue extremely rapidly. Myostatin deficiency shifts muscle from aerobic toward anaerobic energy metabolism, as evidenced by decreased mitochondrial respiration, reduced expression of PPAR transcriptional regulators, increased enolase activity, and exercise-induced lactic acidosis. As a consequence, constitutively reduced myostatin signaling diminishes exercise capacity, while the hypermuscular state of Mstn/ mice increases oxygen consumption and the energy cost of running. We wondered whether these results are the mere consequence of the congenital fiber-type switch toward a glycolytic phenotype of constitutive Mstn/ mice. Hence, we overexpressed myostatin propeptide in adult mice, which did not affect fiber-type distribution, while nonetheless causing increased muscle fatigability, diminished exercise capacity, and decreased Pparb/d and Pgc1a expression. In conclusion, our results suggest that myostatin endows skeletal muscle with high oxidative capacity and low fatigability, thus regulating the delicate balance between muscle mass, muscle force, energy metabolism, and endurance capacity.

Published
2014

119. Dystrophin restoration therapy improves both the reduced excitability and the force drop induced by lengthening contractions in dystrophic mdx skeletal muscle

Author

Roy, Pauline, primary, Rau, Fredérique, additional, Ochala, Julien, additional, Messéant, Julien, additional, Fraysse, Bodvael, additional, Lainé, Jeanne, additional, Agbulut, Onnik, additional, Butler-Browne, Gillian, additional, Furling, Denis, additional, and Ferry, Arnaud, additional

Published
2016
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122. Efficacy of Epicardially Delivered Adipose Stromal Cell Sheets in Dilated Cardiomyopathy

Author

Hamdi, Hadhami, Roitard, Solene, Planat-Benard, Valerie, Pouly, Julia, Nematalla, Hany, Joanne, Pierre, Perier, Marie-Cecile, Bellamv, Valerie, Casteilla, Louis, Li, Zhenlin, Mathias MERICSKAY, Menasche, Philippe, Agbulut, Onnik, Génétique et Physiopathologie des Tissus Musculaires (GPTM), Adaptation Biologique et Vieillissement = Biological Adaptation and Ageing (B2A), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-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)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-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), Cellules Souches et Biothérapies (CSB), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-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)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-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), and HAL-UPMC, Gestionnaire

Subjects
[SDV] Life Sciences [q-bio], Stem cell therapy, Cardiomyopathy, Cells, [SDV]Life Sciences [q-bio], Transplantation/surgical aspects, Stem/progenitor cells, ComputingMilieux_MISCELLANEOUS
Abstract

International audience; no abstract

Published
2012

123. Abstract 11548: Nanofibrous Collagen Scaffolds Seeded With Human Pluripotent Stem Cell-derived Cardiomyocytes Induce Cardiac Remodeling in Dilated Cardiomyopathy

Author

Boitard, Solene, primary, Joanne, Pierre, additional, Kitsara, Maria, additional, Nematalla, Hany, additional, Vanneaux, Valérie, additional, Pernot, Mathieu, additional, Larghero, Jerome, additional, Forest, Patricia, additional, Chen, Yong, additional, Menasché, Philippe, additional, and Agbulut, Onnik, additional

Published
2015
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124. Long-term functional benefits of human embryonic stem cell-derived cardiac progenitors embedded into a fibrin scaffold

Author

Bellamy, Valérie, primary, Vanneaux, Valérie, additional, Bel, Alain, additional, Nemetalla, Hany, additional, Emmanuelle Boitard, Solène, additional, Farouz, Yohan, additional, Joanne, Pierre, additional, Perier, Marie-Cécile, additional, Robidel, Estelle, additional, Mandet, Chantal, additional, Hagège, Albert, additional, Bruneval, Patrick, additional, Larghero, Jérôme, additional, Agbulut, Onnik, additional, and Menasché, Philippe, additional

Published
2015
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127. Towards a clinical use of human embryonic stem cell-derived cardiac progenitors: a translational experience

Author

Menasché, Philippe, primary, Vanneaux, Valérie, additional, Fabreguettes, Jean-Roch, additional, Bel, Alain, additional, Tosca, Lucie, additional, Garcia, Sylvie, additional, Bellamy, Valérie, additional, Farouz, Yohan, additional, Pouly, Julia, additional, Damour, Odile, additional, Périer, Marie-Cécile, additional, Desnos, Michel, additional, Hagège, Albert, additional, Agbulut, Onnik, additional, Bruneval, Patrick, additional, Tachdjian, Gérard, additional, Trouvin, Jean-Hugues, additional, and Larghero, Jérôme, additional

Published
2014
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130. Long-Term Functional Benefits of Epicardial Patches as Cell Carriers

Author

Hamdi, Hadhami, primary, Planat-Benard, Valérie, additional, Bel, Alain, additional, Neamatalla, Hany, additional, Saccenti, Laetitia, additional, Calderon, Damelys, additional, Bellamy, Valérie, additional, Bon, Martin, additional, Perrier, Marie-Cécile, additional, Mandet, Chantal, additional, Bruneval, Patrick, additional, Casteilla, Louis, additional, Hagège, Albert A., additional, Pucéat, Michel, additional, Agbulut, Onnik, additional, and Menasché, Philippe, additional

Published
2014
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131. Correction:Impaired adaptive response to mechanical overloading in dystrophic skeletal muscle (PLoS ONE)

Author

Joanne, Pierre, Hourdé, Christophe, Ochala, Julien, Caudéran, Yvain, Medja, Fadia, Vignaud, Alban, Mouisel, Etienne, Hadj-Said, Wahiba, Arandel, Ludovic, Garcia, Luis, Goyenvalle, Aurélie, Mounier, Rémi, Zibroba, Daria, Sakamato, Kei, Butler-Browne, Gillian, Agbulut, Onnik, Ferry, Arnaud, Joanne, Pierre, Hourdé, Christophe, Ochala, Julien, Caudéran, Yvain, Medja, Fadia, Vignaud, Alban, Mouisel, Etienne, Hadj-Said, Wahiba, Arandel, Ludovic, Garcia, Luis, Goyenvalle, Aurélie, Mounier, Rémi, Zibroba, Daria, Sakamato, Kei, Butler-Browne, Gillian, Agbulut, Onnik, and Ferry, Arnaud

Published
2013

134. Impaired Adaptive Response to Mechanical Overloading in Dystrophic Skeletal Muscle

Author

Joanne, Pierre, Hourdé, Christophe, Ochala, Julien, Caudéran, Yvain, Medja, Fadia, Vignaud, Alban, Mouisel, Etienne, Hadj-Said, Wahiba, Arandel, Ludovic, Garcia, Luis, Goyenvalle, Aurelie, Mounier, Remi, Zibroba, Daria, Sakamato, Kei, Butler-Browne, Gillian, Agbulut, Onnik, Ferry, Arnaud, Joanne, Pierre, Hourdé, Christophe, Ochala, Julien, Caudéran, Yvain, Medja, Fadia, Vignaud, Alban, Mouisel, Etienne, Hadj-Said, Wahiba, Arandel, Ludovic, Garcia, Luis, Goyenvalle, Aurelie, Mounier, Remi, Zibroba, Daria, Sakamato, Kei, Butler-Browne, Gillian, Agbulut, Onnik, and Ferry, Arnaud

Abstract

Dystrophin contributes to force transmission and has a protein-scaffolding role for a variety of signaling complexes in skeletal muscle. In the present study, we tested the hypothesis that the muscle adaptive response following mechanical overloading (ML) would be decreased in MDX dystrophic muscle lacking dystrophin. We found that the gains in muscle maximal force production and fatigue resistance in response to ML were both reduced in MDX mice as compared to healthy mice. MDX muscle also exhibited decreased cellular and molecular muscle remodeling (hypertrophy and promotion of slower/oxidative fiber type) in response to ML, and altered intracellular signalings involved in muscle growth and maintenance (mTOR, myostatin, follistatin, AMPK alpha 1, REDD1, atrogin-1, Bnip3). Moreover, dystrophin rescue via exon skipping restored the adaptive response to ML. Therefore our results demonstrate that the adaptive response in response to ML is impaired in dystrophic MDX muscle, most likely because of the dystrophin crucial role.

Published
2012
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135. Smooth muscle cell-specific knock-out of CTIP2 gene results in aortic hemorrhage.

Author

Parlakian, Ara, Blanc, Jocelyne, GAO-Li, Jacqueline, Regnault, Véronique, Agbulut, Onnik, Lacolley, Patrick, and Zhenlin Li

Subjects
SMOOTH muscle, HEMORRHAGE, SINGLE nucleotide polymorphisms
Abstract

Background: Ctip2/Bcl11b is a transcription factor with dual action (repression/activation) that couples epigenetic regulation to gene transcription in a variety of physiological responses under healthy and pathological conditions of various tissues. Single nucleotide polymorphisms of Ctip2/Bcl11b gene are associated with a higher susceptibility for aortic stiffness (1). although Ctip2/Bcl11b has been proposed as a crucial regulator of aortic smooth muscle function (2), its mechanism of action in smooth muscle cells is still to be uncovered. Methods: Morphological, cellular and molecular analysis were carried out on the arteries of smooth muscle cell-specific Ctip2-knockout (KO) mice at 3, 7, 28 days after tamoxifen injections. Results: There is no difference between control and mutant mice at the macroscopic level 3 days after Ctip2 KO induction, however, 7 day after Bcl11b inactivation, 65% of the Ctip2-SMKO mice showed signs of hemorrhage in the distal part of the thoracic aorta near the abdominal aorta. The histological examination of thoracic aorta at 7 indicated the presence of "bumpy region" in the mutant aorta. These areas is covered by a thicker layer of extracellular matrix and the presence of IgG positive cells, indicating that cell death is occurring. However, the hemorrhages is contained over time, do not impact mice survival. qPCR analysis indicated the altered expression of circadian-related genes such as genes of Bmal and ciart. Conclusions: Our data indicate the primary effect of Bcl11b inactivation on cell death, probably by necroptosis. [ABSTRACT FROM AUTHOR]

Published
2023
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137. Correction: Impaired Adaptive Response to Mechanical Overloading in Dystrophic Skeletal Muscle

Author

Joanne, Pierre, primary, Hourdé, Christophe, additional, Ochala, Julien, additional, Caudéran, Yvain, additional, Medja, Fadia, additional, Vignaud, Alban, additional, Mouisel, Etienne, additional, Hadj-Said, Wahiba, additional, Arandel, Ludovic, additional, Garcia, Luis, additional, Goyenvalle, Aurélie, additional, Mounier, Rémi, additional, Zibroba, Daria, additional, Sakamato, Kei, additional, Butler-Browne, Gillian, additional, Agbulut, Onnik, additional, and Ferry, Arnaud, additional

Published
2013
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139. Impaired Adaptive Response to Mechanical Overloading in Dystrophic Skeletal Muscle

Author

Joanne, Pierre, primary, Hourdé, Christophe, additional, Ochala, Julien, additional, Caudéran, Yvain, additional, Medja, Fadia, additional, Vignaud, Alban, additional, Mouisel, Etienne, additional, Hadj-Said, Wahiba, additional, Arandel, Ludovic, additional, Garcia, Luis, additional, Goyenvalle, Aurélie, additional, Mounier, Rémi, additional, Zibroba, Daria, additional, Sakamato, Kei, additional, Butler-Browne, Gillian, additional, Agbulut, Onnik, additional, and Ferry, Arnaud, additional

Published
2012
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144. Characterization of the paracrine effects of human skeletal myoblasts transplanted in infarcted myocardium

Author

Perez‐Ilzarbe, Maitane, primary, Agbulut, Onnik, additional, Pelacho, Beatriz, additional, Ciorba, Cristina, additional, Jose‐Eneriz, Edurne San, additional, Desnos, Michel, additional, Hagège, Albert A., additional, Aranda, Pablo, additional, Andreu, Enrique J., additional, Menasché, Philippe, additional, and Prósper, Felipe, additional

Published
2008
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