المؤلفون: Gary J. He, Aurélien Corneau, Tom H. Cheung, Elisa Negroni, Hiroshi Sakai, M. Mona Siu, Raymond Wan, Shahragim Tajbakhsh, Lorenzo Giordani, Justin Y. C. Law, Fabien Le Grand

المساهمون: Centre de recherche en Myologie – U974 SU-INSERM, Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Hong Kong University of Science and Technology (HKUST), Cellules Souches et Développement / Stem Cells and Development, Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), Max Planck Institute for Heart and Lung Research (MPI-HLR), Max-Planck-Gesellschaft, Plateforme Cytométrie Pitié-Salpêtrière (LUMIC-CYPS), Unité Mixte de Service d'Imagerie et de Cytométrie [CHU Saint-Antoine] (UMS LUMIC), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), This study was supported by ANR/RGC (Agence Nationale pour la Recherche/Research Grant Council) grant ANR-14-CE11-0026/A-HKUST604/14 (to F.L.G. and T.C.), an Association Française contre les Myopathies/AFM Telethon grant to F.L.G., the Hong Kong Research Grant Council (research grants C6015-14G, C6003-14G, C6009-15G, AoE/M-604/16, and T13-607/12R to T.H.C.), and the Croucher Innovation Award (T.H.C.)., We thank Catherine Blanc (CyPS Facility) for technical support. We thank Bruno Cadot, Christophe Combadière, Glenda Comai, and Vincent Mouly for providing transgenic mice. We thank Gilian Butler-Browne, Florian Bentzinger, David Sassoon, Rémi Mounier, and Capucine Trollet for commenting on the manuscript., Centre de Recherche en Myologie, Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Unité Mixte de Service d'Imagerie et de Cytométrie [CHU Saint-Antoine] (UMS LUMIC), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)

المصدر: Molecular Cell
Molecular Cell, Elsevier, 2019, 74 (3), pp.609-621.e6. ⟨10.1016/j.molcel.2019.02.026⟩
Molecular Cell, 2019, 74 (3), pp.609-621.e6. ⟨10.1016/j.molcel.2019.02.026⟩

مصطلحات موضوعية: MESH: Muscle Fibers, Skeletal/metabolism, Cell type, MESH: Muscle Fibers, Skeletal/cytology, Satellite Cells, Skeletal Muscle, [SDV]Life Sciences [q-bio], Cell, Muscle Fibers, Skeletal, skeletal muscle stem cells, Biology, Muscle Development, Myoblasts, 03 medical and health sciences, Mice, 0302 clinical medicine, MESH: Stem Cells/metabolism, medicine, Compartment (development), MESH: Myoblasts/metabolism, MESH: Satellite Cells, Skeletal Muscle/metabolism, Animals, MESH: Animals, Cell Lineage, MESH: Satellite Cells, Skeletal Muscle/cytology, MESH: Cell Lineage/genetics, Molecular Biology, MESH: Mice, 030304 developmental biology, satellite cells, 0303 health sciences, single-cell RNA-seq, Regeneration (biology), MESH: Cell Differentiation/genetics, Stem Cells, Mesenchymal stem cell, Scleraxis, MESH: Myoblasts/cytology, Skeletal muscle, Cell Differentiation, Cell Biology, Cell biology, Transplantation, MESH: Stem Cells/cytology, medicine.anatomical_structure, MESH: Muscle Development/genetics, CyTOF, Single-Cell Analysis, 030217 neurology & neurosurgery, MESH: Single-Cell Analysis

الوصف: International audience; Adult tissue repair and regeneration require stem-progenitor cells that can self-renew and generate differentiated progeny. Skeletal muscle regenerative capacity relies on muscle satellite cells (MuSCs) and their interplay with different cell types within the niche. However, our understanding of skeletal muscle tissue cellular composition is limited. Here, using a combined approach of single-cell RNA sequencing and mass cytometry, we precisely mapped 10 different mononuclear cell types in adult mouse muscle. We also characterized gene signatures and determined key discriminating markers of each cell type. We identified two previously understudied cell populations in the interstitial compartment. One expresses the transcription factor scleraxis and generated tenocytes in vitro. The second expresses markers of smooth muscle and mesenchymal cells (SMMCs) and, while distinct from MuSCs, exhibited myogenic potential and promoted MuSC engraftment following transplantation. The blueprint presented here yields crucial insights into muscle-resident cell-type identities and can be exploited to study muscle diseases.

URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::8b39aea4fb8ca4e7185adbe7f87a1f19
https://pubmed.ncbi.nlm.nih.gov/30922843

المؤلفون: Ellis Gielen, Anita Kneppers, Luc J. C. van Loon, Chiel C. de Theije, Ramon C. J. Langen, Mark Corten, Annemie M. W. J. Schols, Lex B. Verdijk

المساهمون: Pulmonologie, RS: NUTRIM - R3 - Respiratory & Age-related Health, Promovendi NTM, Humane Biologie, Ondersteunend personeel NTM

المصدر: Skeletal Muscle, Vol 8, Iss 1, Pp 1-13 (2018)
Skeletal Muscle
Skeletal Muscle, 8:4. BioMed Central Ltd

مصطلحات موضوعية: 0301 basic medicine, postnatal myogenesis, MUSCLE STEM-CELLS, lcsh:Diseases of the musculoskeletal system, MYOTUBE HYPERTROPHY, Cellular differentiation, Muscle Fibers, Skeletal, Interleukin-4/pharmacology, Cell, Muscle Proteins, Myostatin, Muscle Development, Mice, Myoblast fusion, FIBER HYPERTROPHY, Models, muscle repair, Myocyte, Orthopedics and Sports Medicine, Insulin-Like Growth Factor I, Muscle Development/drug effects, Cells, Cultured, Muscle Proteins/metabolism, satellite cells, muscle regeneration, Interleukin-13, Cultured, biology, Myogenesis, myoblasts, Muscle Fibers, Skeletal/cytology, REGENERATIVE MYOGENESIS, HUMAN SKELETAL-MUSCLE, TNF-ALPHA, Cell biology, medicine.anatomical_structure, MYOBLAST FUSION, Skeletal/cytology, DIGITORUM LONGUS MUSCLE, Insulin-Like Growth Factor I/pharmacology, Muscle, C2C12, Signal Transduction, Interleukin-13/pharmacology, Regeneration/drug effects, Cells, Models, Biological, Muscle Fibers, 03 medical and health sciences, Skeletal/physiology, medicine, Regeneration, Humans, Animals, skeletal muscle, Muscle, Skeletal, Molecular Biology, cell fusion, Signal Transduction/physiology, Methodology, Membrane Proteins, Skeletal muscle, Cell Biology, Biological, muscle maintenance, Coculture Techniques, Muscle, Skeletal/physiology, cell differentiation, 030104 developmental biology, myotubes, Cell Differentiation/drug effects, biology.protein, Membrane Proteins/metabolism, Interleukin-4, lcsh:RC925-935, GAMMA-IRRADIATION, Atrophy, Myoblasts/cytology

الوصف: Background Due to the post-mitotic nature of myonuclei, postnatal myogenesis is essential for skeletal muscle growth, repair, and regeneration. This process is facilitated by satellite cells through proliferation, differentiation, and subsequent fusion with a pre-existing muscle fiber (i.e., myonuclear accretion). Current knowledge of myogenesis is primarily based on the in vitro formation of syncytia from myoblasts, which represents aspects of developmental myogenesis, but may incompletely portray postnatal myogenesis. Therefore, we aimed to develop an in vitro model that better reflects postnatal myogenesis, to study the cell intrinsic and extrinsic processes and signaling involved in the regulation of postnatal myogenesis. Methods Proliferating C2C12 myoblasts were trypsinized and co-cultured for 3 days with 5 days differentiated C2C12 myotubes. Postnatal myonuclear accretion was visually assessed by live cell time-lapse imaging and cell tracing by cell labeling with Vybrant® DiD and DiO. Furthermore, a Cre/LoxP-based cell system was developed to semi-quantitatively assess in vitro postnatal myonuclear accretion by the conditional expression of luciferase upon myoblast–myotube fusion. Luciferase activity was assessed luminometrically and corrected for total protein content. Results Live cell time-lapse imaging, staining-based cell tracing, and recombination-dependent luciferase activity, showed the occurrence of postnatal myonuclear accretion in vitro. Treatment of co-cultures with the myogenic factor IGF-I (p

وصف الملف: application/pdf

URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::87156d3fc968b0798d2685a4c5e60989
https://acuresearchbank.acu.edu.au/item/8845w/a-novel-in-vitro-model-for-the-assessment-of-postnatal-myonuclear-accretion

المؤلفون: Michel Fardeau, Laurent Schaeffer, Thierry Kuntzer, Isabelle Grosjean, Daniel Hantaï, A. Rouche, Annie Chaboud, Asma Ben Ammar, Nektaria Alexandri, Frédéric Chevessier, Caroline Huzé, Emmanuel Fournier, Andrea Brancaccio, K. Gaudon, Bruno Eymard, Jeanine Koenig, S. Bauche, Evelyne Goillot, Véronique Bernard, Heba-Aude Lecuyer, Pascale Richard, Markus A. Rüegg

المساهمون: Laboratoire de Biologie Moléculaire de la Cellule ( LBMC ), École normale supérieure - Lyon ( ENS Lyon ) -Université Claude Bernard Lyon 1 ( UCBL ), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Centre de Recherche de l'Institut du Cerveau et de la Moelle épinière ( CRICM ), 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 ), Unité Fonctionnelle de Cardiogénétique et Myogénétique Moléculaire et Cellulaire, Assistance publique - Hôpitaux de Paris (AP-HP)-Centre de Génétique Moléculaire et Chromosomique du GH Pitié-Salpêtrière-CHU Pitié-Salpêtrière [APHP], Max-Planck-Institut für Medizinische Forschung, Max-Planck-Gesellschaft, Institut National de Neurologie, Université Tunis El Manar ( UTM ), Plateau d'analyse des protéines, IFR128, Biologie des Jonctions Neuromusculaires Normales et Pathologiques ( U686 ), Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Nerve-muscle unit, neurology service, Université de Lausanne ( UNIL ) -Centre Hospitalier Universitaire Vaudois [Lausanne] ( CHUV ), Centre de référence des maladies rares neuromusculaires, Assistance publique - Hôpitaux de Paris (AP-HP)-CHU Pitié-Salpêtrière [APHP], Service d'électrophysiologie, Istituto di Chimica del Riconoscimento Molecolare, Università Cattolica del Sacro Cuore, Biozentrum, University of Basel ( Unibas ), ANR-07-MRAR-0001,MRAR,Syndromes myasthéniques congénitaux : le réseau français et approches fondamentales ( 2007 ), Hantaï, Daniel, Programme Pluriannuel de Recherche sur les Maladies Rares (MRAR) - Implication de CXCL13 et CCL21 dans les mécanismes pathogéniques de la Myasthenie. - - MG chemokines2006 - ANR-06-MRAR-0001 - MRAR - VALID, Laboratoire de Biologie Moléculaire de la Cellule (LBMC), École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centre de Recherche de l'Institut du Cerveau et de la Moelle épinière (CRICM), 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), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU), Université de Tunis El Manar (UTM), Biologie des Jonctions Neuromusculaires Normales et Pathologiques (U686), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Neuroscience Paris Seine (NPS), 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)-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), Université de Lausanne = University of Lausanne (UNIL)-Centre Hospitalier Universitaire Vaudois [Lausanne] (CHUV), Centre de référence des maladies rares neuromusculaires [CHU Pitié-Salpétriêre], CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Università cattolica del Sacro Cuore [Milano] (Unicatt), Biozentrum [Basel, Suisse], University of Basel (Unibas), ANR-06-MRAR-0001,MG chemokines,Implication de CXCL13 et CCL21 dans les mécanismes pathogéniques de la Myasthenie.(2006), École normale supérieure de Lyon (ENS de Lyon)-Université Claude Bernard Lyon 1 (UCBL), 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), Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Neurosciences Paris Seine (NPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-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)-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)-Centre National de la Recherche Scientifique (CNRS), Centre Hospitalier Universitaire Vaudois [Lausanne] (CHUV)-Université de Lausanne (UNIL), Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-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)-Sorbonne Université (SU)-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 du Cerveau et de la Moëlle Epinière = Brain and Spine Institute (ICM), 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)-CHU Pitié-Salpêtrière [AP-HP], Sorbonne Université-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Sorbonne Université-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université, 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)-Centre National de la Recherche Scientifique (CNRS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Sorbonne Université-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Centre National de la Recherche Scientifique (CNRS)

المصدر: American Journal of Human Genetics
American Journal of Human Genetics, Elsevier (Cell Press), 2009, 85 (2), pp.155-67. 〈10.1016/j.ajhg.2009.06.015〉
American Journal of Human Genetics, vol. 85, no. 2, pp. 155-167
American Journal of Human Genetics, 2009, 85 (2), pp.155-67. ⟨10.1016/j.ajhg.2009.06.015⟩
American Journal of Human Genetics, Elsevier (Cell Press), 2009, 85 (2), pp.155-67. ⟨10.1016/j.ajhg.2009.06.015⟩
American Journal of Human Genetics, Elsevier (Cell Press), 2009, 85 (2), pp.155-167. ⟨10.1016/j.ajhg.2009.06.015⟩
The American Journal of Human Genetics

مصطلحات موضوعية: Male, Biopsy, DNA Mutational Analysis, Muscle Fibers, Skeletal, Mutant, [SDV.GEN] Life Sciences [q-bio]/Genetics, 0302 clinical medicine, Mutant protein, CHRNE, Receptors, Cholinergic, Genetics(clinical), Dystroglycans, ComputingMilieux_MISCELLANEOUS, Genetics (clinical), Genetics, 0303 health sciences, Agrin, Congenital myasthenic syndrome, Recombinant Proteins, Pedigree, Cell biology, medicine.anatomical_structure, Female, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Dok-7, Adult, animal structures, Mutation, Missense, Neuromuscular Junction, Biology, Article, Neuromuscular junction, Cell Line, 03 medical and health sciences, medicine, Animals, Humans, [SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Muscle, Skeletal, 030304 developmental biology, Acetylcholine receptor, Myasthenic Syndromes, Congenital, [SDV.GEN]Life Sciences [q-bio]/Genetics, Correction, medicine.disease, Protein Structure, Tertiary, Rats, Models, Chemical, [ SDV.NEU ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Synapses, 030221 ophthalmology & optometry, biology.protein, Agrin/chemistry, Agrin/genetics, Dystroglycans/metabolism, Muscle Fibers, Skeletal/cytology, Muscle Fibers, Skeletal/metabolism, Muscle, Skeletal/metabolism, Muscle, Skeletal/pathology, Myasthenic Syndromes, Congenital/genetics, Neuromuscular Junction/genetics, Neuromuscular Junction/metabolism, Receptors, Cholinergic/genetics, Receptors, Cholinergic/metabolism, Recombinant Proteins/chemistry, Recombinant Proteins/metabolism, Synapses/metabolism, [ SDV.GEN ] Life Sciences [q-bio]/Genetics, 030217 neurology & neurosurgery

الوصف: International audience; We report the case of a congenital myasthenic syndrome due to a mutation in AGRN, the gene encoding agrin, an extracellular matrix molecule released by the nerve and critical for formation of the neuromuscular junction. Gene analysis identified a homozygous missense mutation, c.5125G>C, leading to the p.Gly1709Arg variant. The muscle-biopsy specimen showed a major disorganization of the neuromuscular junction, including changes in the nerve-terminal cytoskeleton and fragmentation of the synaptic gutters. Experiments performed in nonmuscle cells or in cultured C2C12 myotubes and using recombinant mini-agrin for the mutated and the wild-type forms showed that the mutated form did not impair the activation of MuSK or change the total number of induced acetylcholine receptor aggregates. A solid-phase assay using the dystrophin glycoprotein complex showed that the mutation did not affect the binding of agrin to alpha-dystroglycan. Injection of wild-type or mutated agrin into rat soleus muscle induced the formation of nonsynaptic acetylcholine receptor clusters, but the mutant protein specifically destabilized the endogenous neuromuscular junctions. Importantly, the changes observed in rat muscle injected with mutant agrin recapitulated the pre- and post-synaptic modifications observed in the patient. These results indicate that the mutation does not interfere with the ability of agrin to induce postsynaptic structures but that it dramatically perturbs the maintenance of the neuromuscular junction.

وصف الملف: application/pdf

URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::310ffa6794cb81a011a830a4c22a3e01
https://doi.org/10.1016/j.ajhg.2009.06.015

المؤلفون: Jacqueline Fischer-Lougheed, Charles R. Bader, Laurent Bernheim, Estelle Espinos, Dominique Belin, Jian-Hui Liu, David Mordasini

المصدر: The Journal of Cell Biology
The Journal of Cell Biology, Vol. 153, No 4 (2001) pp. 677-686

مصطلحات موضوعية: Patch-Clamp Techniques, Potassium Channels, muscle, antisense, Muscle, Skeletal/ cytology/physiology, Muscle Fibers, Skeletal, Potassium/metabolism, Biology, In Vitro Techniques, Membrane Fusion, Membrane Potentials, Myoblast fusion, Ribonucleases, potassium current, myoblast fusion, medicine, Myocyte, Humans, Patch clamp, Potassium Channels, Inwardly Rectifying, Child, Muscle, Skeletal, Muscle Fibers, Skeletal/ cytology, Membrane potential, Inward-rectifier potassium ion channel, Comment, Lipid bilayer fusion, Skeletal muscle, Infant, Cell Differentiation, Cell Biology, Anatomy, Hyperpolarization (biology), musculoskeletal system, ddc:616.8, Cell biology, medicine.anatomical_structure, Antisense Elements (Genetics), Membrane Potentials/physiology, Child, Preschool, Membrane Fusion/physiology, Potassium, Original Article, membrane potential, tissues, Potassium Channels/ genetics/ metabolism

الوصف: Myoblast fusion is essential to skeletal muscle development and repair. We have demonstrated previously that human myoblasts hyperpolarize, before fusion, through the sequential expression of two K+ channels: an ether-à-go-go and an inward rectifier. This hyperpolarization is a prerequisite for fusion, as it sets the resting membrane potential in a range at which Ca2+ can enter myoblasts and thereby trigger fusion via a window current through α1H T channels.

URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::3ca7053bbfbf8487050a011efddfbd00
https://pubmed.ncbi.nlm.nih.gov/11352947

المؤلفون: C. Garbarsch, Torsten Deckert, Jhm Berden, Pernille M. Hansen, Hiroki Yokoyama, P.E. Hoyer, J. van den Born, Tonny Jensen

المساهمون: Groningen Kidney Center (GKC), Groningen Institute for Organ Transplantation (GIOT)

المصدر: Diabetes, 46, pp. 1875-1880
Diabetes, 46, 1875-1880
Diabetes, 46, 11, pp. 1875-1880
Diabetes, 46(11), 1875-1880. AMER DIABETES ASSOC

مصطلحات موضوعية: Male, Heparan Sulfate Proteoglycans/analysis, Endocrinology, Diabetes and Metabolism, Muscle Fibers, Skeletal, Blood Pressure, Collagen/analysis, Basement Membrane/cytology, Basement Membrane, Muscle, Smooth, Vascular, Diabetic nephropathy, chemistry.chemical_compound, Reference Values, Diabetic Nephropathies, Age of Onset, GeneralLiterature_REFERENCE(e.g.,dictionaries,encyclopedias,glossaries), Prevention of diabetic nephropathy by modulation of growth factor induced extracellular matrix alterations, biology, Creatinine/metabolism, Skeletal/blood supply, Muscle Fibers, Skeletal/cytology, Heparan sulfate, Vascular/cytology, Type 1/pathology, medicine.anatomical_structure, Muscle, Smooth, Vascular/cytology, Skeletal/cytology, Creatinine, Muscle, Regression Analysis, Female, Collagen, Smooth, medicine.symptom, Adult, medicine.medical_specialty, Capillaries/cytology, Preventie van diabetische nefropathie door modulatie van groeifaktor-geinduceerde extracellulaire matrix veranderingen, Renal function, Muscle Fibers, Internal medicine, medicine, Internal Medicine, Diabetes Mellitus, Albuminuria, Humans, Muscle, Skeletal, Basement membrane, Diabetic Nephropathies/pathology, Diabetes Mellitus, Type 1/pathology, Skeletal muscle, medicine.disease, Capillaries, Endocrinology, Diabetes Mellitus, Type 1, Proteoglycan, chemistry, biology.protein, Glomerular Filtration Barrier, Muscle, Skeletal/blood supply, Heparan Sulfate Proteoglycans

الوصف: In IDDM patients, an increased permeability of the glomerular capillaries has been associated with a general loss of negatively charged heparan sulfate proteoglycans (HSPGs) within basement membranes (BMs). In the present study, we used immunohistochemical staining to quantify heparan sulfate (HS), HSPG core protein, and collagen IV in capillary basement membranes of skeletal muscle biopsies taken from 9 healthy control subjects (C) and 20 IDDM patients: 7 with normal albumin excretion rate (300 mg/24 h) (D2). In the capillaries, staining was measured by a scanning and integrating microspectrophotometer. A significant difference in the absorbance of HS was found among the four subgroups (means +/- SD): 0.477 +/- 0.082 (C), 0.627 +/- 0.031 (D0), 0.542 +/- 0.098 (D1), and 0.371 +/- 0.118 (D2) (P = 0.006). Similarly, an overall significant difference in the absorbance of collagen IV was demonstrated (means +/- SD): 0.836 +/- 0.111 (C), 0.838 +/- 0.300 (D0), 0.970 +/- 0.173 (D1), and 0.512 +/- 0.248 (D2) (P = 0.02). No statistical difference in the absorbance of core protein was demonstrated among the groups. Within the diabetic groups, HS was inversely correlated to albuminuria (r = -0.76, P = 0.003) and albuminuria corrected for creatinine clearance (r = -0.69, P = 0.008). Because, in IDDM patients with albuminuria, alterations of the content of HS and collagen IV within the capillary BM have been demonstrated immunohistochemically, not only in the glomerular filtration barrier, but also in the skeletal muscle capillary BM, we suggest that these changes reflect universal quantitative or qualitative alterations within the capillary filtration barrier.

وصف الملف: application/pdf

URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::588c5b844a632b87e256c4effd52cf19
https://hdl.handle.net/2066/222734

المؤلفون: Zarko Grozdanovic, Reinhart Gossrau, Gudrun Dahrmann, Georgios Nakos, Bernd Mayer

مصطلحات موضوعية: Male, Histology, Somatic cell, Muscle Fibers, Skeletal, Guinea Pigs, Myosins/analysis, Nitric Oxide Synthase/analysis/*biosynthesis, Hamster, Fluorescent Antibody Technique, Mice, Inbred Strains, Biology, Myosins, Pathology and Forensic Medicine, Nitric oxide, Guinea pig, chemistry.chemical_compound, Mice, Sarcolemma, NADPH Dehydrogenase/analysis, Sarcolemma/*enzymology/ultrastructure, Species Specificity, Cricetinae, Myosin, Muscle Fibers, Skeletal/cytology/*enzymology, Animals, Rats, Wistar, Muscle, Skeletal, Muscle, Smooth/cytology/enzymology, NADPH Dehydrogenase, Muscle, Smooth, Callithrix, Cell Biology, Molecular biology, Staining, Rats, Nitric oxide synthase, Biochemistry, chemistry, Organ Specificity, biology.protein, Female, Muscle, Skeletal/cytology/enzymology, Nitric Oxide Synthase, Gerbillinae

الوصف: The expression and distribution of nitric oxide synthase (NOS) was studied by use of the newly designed specific histochemical NADPH diaphorase staining method and the indirect immunofluorescence technique employing an antiserum to brain NOS in visceral and somatic striated muscles of several mammalian species. Histochemical activity and immunoreactivity were located in the sarcolemma region of type I and II fibers of all muscles investigated. Visceral muscles were more strongly stained than somatic muscles. Furthermore, type II fibers, identified by staining of myosin adenosine triphosphatase activity after pre-incubation at alkaline pH, were more intensely labeled than type I fibers. In addition, NOS activity was detected in the area of the sarcolemma of intrafusal fibers. No obvious differences between species were observed. It was concluded that NOS of striated muscles probably makes up the richest and most important nitric oxide source in mammals. Cell Tissue Res

URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::da547b5b8eb13a6c95f30b94a3310471
http://olympias.lib.uoi.gr/jspui/handle/123456789/18180

مستخلص: Background: Postsynaptic enrichment of acetylcholine receptors (AChRs) at the vertebrate neuromuscular junction (NMJ) depends on the activation of the muscle receptor tyrosine MuSK by neural agrin. Agrin-stimulation of MuSK is known to initiate an intracellular signaling cascade that leads to the clustering of AChRs in an actin polymerization-dependent manner, but the molecular steps which link MuSK activation to AChR aggregation remain incompletely defined. Methodology/Principal Findings: In this study we used biochemical, cell biological and molecular assays to investigate a possible role in AChR clustering of cortactin, a protein which is a tyrosine kinase substrate and a regulator of F-actin assembly and which has also been previously localized at AChR clustering sites. We report that cortactin was co-enriched at AChR clusters in situ with its target the Arp2/3 complex, which is a key stimulator of actin polymerization in cells. Cortactin was further preferentially tyrosine phosphorylated at AChR clustering sites and treatment of myotubes with agrin significantly enhanced the tyrosine phosphorylation of cortactin. Importantly, forced expression in myotubes of a tyrosine phosphorylation-defective cortactin mutant (but not wild-type cortactin) suppressed agrin-dependent AChR clustering, as did the reduction of endogenous cortactin levels using RNA interference, and introduction of the mutant cortactin into muscle cells potently inhibited synaptic AChR aggregation in response to innervation. Conclusion: Our results suggest a novel function of phosphorylation-dependent cortactin signaling downstream from agrin/MuSK in facilitating AChR clustering at the developing NMJ.

مصطلحات الفهرس: Actin-Related Protein 2-3 Complex: metabolism, Actins: metabolism, Agrin: pharmacology, Animals, Cell Line, Cortactin: metabolism, Humans, Mice, Models, Biological, Muscle Fibers, Skeletal: cytology, Muscle Fibers, Skeletal: drug effects, Muscle Fibers, Skeletal: metabolism, Mutation: genetics, Neuromuscular Junction: cytology, Neuromuscular Junction: drug effects, Neuromuscular Junction: metabolism, Phosphorylation: drug effects, Phosphotyrosine: metabolism, Receptors, Cholinergic: metabolism, Signal Transduction: drug effects, Vertebrates: metabolism, Xenopus, Article

URL: https://repository.hkust.edu.hk/ir/Record/1783.1-30995
https://doi.org/10.1371/journal.pone.0008478
http://lbdiscover.ust.hk/uresolver?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rfr_id=info:sid/HKUST:SPI&rft.genre=article&rft.issn=1932-6203&rft.volume=4&rft.issue=12&rft.date=2009&rft.spage=&rft.aulast=Madhavan&rft.aufirst=Raghavan&rft.atitle=The+Function+of+Cortactin+in+the+Clustering+of+Acetylcholine+Receptors+at+the+Vertebrate+Neuromuscular+Junction
http://gateway.isiknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=LinksAMR&SrcApp=PARTNER_APP&DestLinkType=FullRecord&DestApp=WOS&KeyUT=000273105200013
http://www.scopus.com/record/display.url?eid=2-s2.0-77949507489&origin=inward

مستخلص: Background: Postsynaptic enrichment of acetylcholine receptors (AChRs) at the vertebrate neuromuscular junction (NMJ) depends on the activation of the muscle receptor tyrosine MuSK by neural agrin. Agrin-stimulation of MuSK is known to initiate an intracellular signaling cascade that leads to the clustering of AChRs in an actin polymerization-dependent manner, but the molecular steps which link MuSK activation to AChR aggregation remain incompletely defined. Methodology/Principal Findings: In this study we used biochemical, cell biological and molecular assays to investigate a possible role in AChR clustering of cortactin, a protein which is a tyrosine kinase substrate and a regulator of F-actin assembly and which has also been previously localized at AChR clustering sites. We report that cortactin was co-enriched at AChR clusters in situ with its target the Arp2/3 complex, which is a key stimulator of actin polymerization in cells. Cortactin was further preferentially tyrosine phosphorylated at AChR clustering sites and treatment of myotubes with agrin significantly enhanced the tyrosine phosphorylation of cortactin. Importantly, forced expression in myotubes of a tyrosine phosphorylation-defective cortactin mutant (but not wild-type cortactin) suppressed agrin-dependent AChR clustering, as did the reduction of endogenous cortactin levels using RNA interference, and introduction of the mutant cortactin into muscle cells potently inhibited synaptic AChR aggregation in response to innervation. Conclusion: Our results suggest a novel function of phosphorylation-dependent cortactin signaling downstream from agrin/MuSK in facilitating AChR clustering at the developing NMJ.

مصطلحات الفهرس: Actin-Related Protein 2-3 Complex: metabolism, Actins: metabolism, Agrin: pharmacology, Animals, Cell Line, Cortactin: metabolism, Humans, Mice, Models, Biological, Muscle Fibers, Skeletal: cytology, Muscle Fibers, Skeletal: drug effects, Muscle Fibers, Skeletal: metabolism, Mutation: genetics, Neuromuscular Junction: cytology, Neuromuscular Junction: drug effects, Neuromuscular Junction: metabolism, Phosphorylation: drug effects, Phosphotyrosine: metabolism, Receptors, Cholinergic: metabolism, Signal Transduction: drug effects, Vertebrates: metabolism, Xenopus, Article

URL: http://repository.ust.hk/ir/Record/1783.1-30995
http://lbdiscover.ust.hk/uresolver?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rfr_id=info:sid/HKUST:SPI&rft.genre=article&rft.issn=1932-6203&rft.volume=4&rft.issue=12&rft.date=2009&rft.spage=&rft.aulast=Madhavan&rft.aufirst=Raghavan&rft.atitle=The+Function+of+Cortactin+in+the+Clustering+of+Acetylcholine+Receptors+at+the+Vertebrate+Neuromuscular+Junction
http://gateway.isiknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=LinksAMR&SrcApp=PARTNER_APP&DestLinkType=FullRecord&DestApp=WOS&KeyUT=000273105200013
http://www.scopus.com/record/display.url?eid=2-s2.0-77949507489&origin=inward

مستخلص: Background: Postsynaptic enrichment of acetylcholine receptors (AChRs) at the vertebrate neuromuscular junction (NMJ) depends on the activation of the muscle receptor tyrosine MuSK by neural agrin. Agrin-stimulation of MuSK is known to initiate an intracellular signaling cascade that leads to the clustering of AChRs in an actin polymerization-dependent manner, but the molecular steps which link MuSK activation to AChR aggregation remain incompletely defined. Methodology/Principal Findings: In this study we used biochemical, cell biological and molecular assays to investigate a possible role in AChR clustering of cortactin, a protein which is a tyrosine kinase substrate and a regulator of F-actin assembly and which has also been previously localized at AChR clustering sites. We report that cortactin was co-enriched at AChR clusters in situ with its target the Arp2/3 complex, which is a key stimulator of actin polymerization in cells. Cortactin was further preferentially tyrosine phosphorylated at AChR clustering sites and treatment of myotubes with agrin significantly enhanced the tyrosine phosphorylation of cortactin. Importantly, forced expression in myotubes of a tyrosine phosphorylation-defective cortactin mutant (but not wild-type cortactin) suppressed agrin-dependent AChR clustering, as did the reduction of endogenous cortactin levels using RNA interference, and introduction of the mutant cortactin into muscle cells potently inhibited synaptic AChR aggregation in response to innervation. Conclusion: Our results suggest a novel function of phosphorylation-dependent cortactin signaling downstream from agrin/MuSK in facilitating AChR clustering at the developing NMJ.

مصطلحات الفهرس: Actin-Related Protein 2-3 Complex: metabolism, Actins: metabolism, Agrin: pharmacology, Animals, Cell Line, Cortactin: metabolism, Humans, Mice, Models, Biological, Muscle Fibers, Skeletal: cytology, Muscle Fibers, Skeletal: drug effects, Muscle Fibers, Skeletal: metabolism, Mutation: genetics, Neuromuscular Junction: cytology, Neuromuscular Junction: drug effects, Neuromuscular Junction: metabolism, Phosphorylation: drug effects, Phosphotyrosine: metabolism, Receptors, Cholinergic: metabolism, Signal Transduction: drug effects, Vertebrates: metabolism, Xenopus, Article

URL: http://repository.ust.hk/ir/Record/1783.1-30995
http://lbdiscover.ust.hk/uresolver?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rfr_id=info:sid/HKUST:SPI&rft.genre=article&rft.issn=1932-6203&rft.volume=4&rft.issue=12&rft.date=2009&rft.spage=&rft.aulast=Madhavan&rft.aufirst=Raghavan&rft.atitle=The+Function+of+Cortactin+in+the+Clustering+of+Acetylcholine+Receptors+at+the+Vertebrate+Neuromuscular+Junction
http://gateway.isiknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=LinksAMR&SrcApp=PARTNER_APP&DestLinkType=FullRecord&DestApp=WOS&KeyUT=000273105200013
http://www.scopus.com/record/display.url?eid=2-s2.0-77949507489&origin=inward

مستخلص: Background: A crucial event in the development of the vertebrate neuromuscular junction (NMJ) is the postsynaptic enrichment of muscle acetylcholine (ACh) receptors (AChRs). This process involves two distinct steps: the local clustering of AChRs at synapses, which depends on the activation of the muscle-specific receptor tyrosine kinase MuSK by neural agrin, and the global dispersal of aneural or "pre-patterned" AChR aggregates, which is triggered by ACh or by synaptogenic stimuli. We and others have previously shown that tyrosine phosphatases, such as the SH2 domain-containing phosphatase Shp2, regulate AChR cluster formation in muscle cells, and that tyrosine phosphatases also mediate the dispersal of pre-patterned AChR clusters by synaptogenic stimuli, although the specific phosphatases involved in this latter step remain unknown. Results: Using an assay system that allows AChR cluster assembly and disassembly to be studied separately and quantitatively, we describe a previously unrecognized role of the tyrosine phosphatase Shp2 in AChR cluster disassembly. Shp2 was robustly expressed in embryonic Xenopus muscle in vivo and in cultured myotomal muscle cells, and treatment of the muscle cultures with an inhibitor of Shp2 (NSC-87877) blocked the dispersal of pre-patterned AChR clusters by synaptogenic stimuli. In contrast, over-expression in muscle cells of either wild-type or constitutively active Shp2 accelerated cluster dispersal. Significantly, forced expression in muscle of the Shp2-activator SIRP alpha 1 (signal regulatory protein alpha 1) also enhanced the disassembly of AChR clusters, whereas the expression of a truncated SIRP alpha 1 mutant that suppresses Shp2 signaling inhibited cluster disassembly. Conclusion: Our results suggest that Shp2 activation by synaptogenic stimuli, through signaling intermediates such as SIRP alpha 1, promotes the dispersal of pre-patterned AChR clusters to facilitate the selective accumulation of AChRs at developing NMJs.

مصطلحات الفهرس: Animals, Antigens, Differentiation: genetics, Antigens, Differentiation: metabolism, Antigens, Differentiation: physiology, Bungarotoxins: pharmacology, Catalytic Domain, Cell Line, Cells, Cultured, Green Fluorescent Proteins: genetics, Green Fluorescent Proteins: metabolism, Humans, Immunoblotting, In Situ Hybridization: methods, Microinjections: methods, Microscopy, Fluorescence, Muscle Fibers, Skeletal: cytology, Muscle Fibers, Skeletal: drug effects, Muscle Fibers, Skeletal: metabolism, Myoblasts: cytology, Myoblasts: metabolism, Neuromuscular Junction: drug effects, Neuromuscular Junction: physiology, Protein Tyrosine Phosphatase, Non-Receptor Type, Article

URL: https://repository.hkust.edu.hk/ir/Record/1783.1-6010
https://doi.org/10.1186/1471-2202-9-70
http://lbdiscover.ust.hk/uresolver?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rfr_id=info:sid/HKUST:SPI&rft.genre=article&rft.issn=1471-2202&rft.volume=9&rft.issue=&rft.date=2008&rft.spage=&rft.aulast=Qian&rft.aufirst=Yueping+K.&rft.atitle=The+function+of+Shp2+tyrosine+phosphatase+in+the+dispersal+of+acetylcholine+receptor+clusters
http://gateway.isiknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=LinksAMR&SrcApp=PARTNER_APP&DestLinkType=FullRecord&DestApp=WOS&KeyUT=000258352100001
http://www.scopus.com/record/display.url?eid=2-s2.0-48349086645&origin=inward
http://repository.ust.hk/ir/bitstream/1783.1-6010/1/186474192008QianYKetalBMPNeurosciShp2andAChRclusterdispersal.pdf