13 results on '"Periou, Baptiste"'
Search Results
2. An up-to-date myopathologic characterisation of facioscapulohumeral muscular dystrophy type 1 muscle biopsies shows sarcolemmal complement membrane attack complex deposits and increased skeletal muscle regeneration
- Author
-
Hubregtse, Lisanne, Bouman, Karlijn, Lama, Chéryane, Lassche, Saskia, de Graaf, Nicolas, Taglietti, Valentina, Küsters, Benno, Periou, Baptiste, Relaix, Frédéric, van Engelen, Baziel, Authier, François-Jerôme, Voermans, Nicol C., and Malfatti, Edoardo
- Published
- 2024
- Full Text
- View/download PDF
3. Duchenne muscular dystrophy trajectory in R-DMDdel52 preclinical rat model identifies COMP as biomarker of fibrosis
- Author
-
Taglietti, Valentina, Kefi, Kaouthar, Bronisz-Budzyńska, Iwona, Mirciloglu, Busra, Rodrigues, Mathilde, Cardone, Nastasia, Coulpier, Fanny, Periou, Baptiste, Gentil, Christel, Goddard, Melissa, Authier, François-Jérôme, Pietri-Rouxel, France, Malfatti, Edoardo, Lafuste, Peggy, Tiret, Laurent, and Relaix, Frederic
- Published
- 2022
- Full Text
- View/download PDF
4. Receptor interacting protein kinase‐3 mediates both myopathy and cardiomyopathy in preclinical animal models of Duchenne muscular dystrophy.
- Author
-
Bencze, Maximilien, Periou, Baptiste, Punzón, Isabel, Barthélémy, Inès, Taglietti, Valentina, Hou, Cyrielle, Zaidan, Louai, Kefi, Kaouthar, Blot, Stéphane, Agbulut, Onnik, Gervais, Marianne, Derumeaux, Geneviève, Authier, François‐Jérôme, Tiret, Laurent, and Relaix, Fréderic
- Published
- 2023
- Full Text
- View/download PDF
5. Interferon-gamma-mediated JAK/STAT1 signalling triggers muscle damage in Inclusion Body Myositis
- Author
-
Hou, Cyrielle, Periou, Baptiste, Gervais, Marianne, Berthier, Juliette, Baba Amer, Yasmine, Malfatti, Edoardo, Souvannanorath, Sarah, Relaix, Fred, Bencze, Maximilien, and Authier, Jérôme
- Published
- 2023
- Full Text
- View/download PDF
6. Automated image-analysis method for the quantification of fiber morphometry and fiber type population in human skeletal muscle
- Author
-
Reyes-Fernandez, Perla C., Periou, Baptiste, Decrouy, Xavier, Relaix, Fréderic, and Authier, François Jérôme
- Published
- 2019
- Full Text
- View/download PDF
7. From diagnosis to prognosis:Revisiting the meaning of muscle ISG15 overexpression in juvenile inflammatory myopathies
- Author
-
Rodero, Mathieu P, Hou, Cyrielle, Durrleman, Chloé, Periou, Baptiste, Barnerias, Christine, Bodemer, Christine, Desguerre, Isabelle, Quartier, Pierre, Melki, Isabelle, Rice, Gillian, Rodero, Mathieu, Charuel, Jean‐Luc, Relaix, Fréderic, Bader‐Meunier, Brigitte, Authier, FrançoisJérôme, Gitiaux, Cyril, Laboratoire de Chimie et de Biochimie Pharmacologiques et Toxicologiques (LCBPT - UMR 8601), Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS)-Université de Paris (UP), Cellules Souches, Plasticité Cellulaire, Médecine Régénératrice et Immunothérapies (IRMB), Université de Montpellier (UM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Imagine - Institut des maladies génétiques (IHU) (Imagine - U1163), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP), Filière Neuromusculaire (FILNEMUS), Service d'immuno-hématologie pédiatrique [CHU Necker], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Necker - Enfants Malades [AP-HP], Service d'Immunologie, hématologie et rhumatologie pédiatriques [Hôpital Necker-Enfants malades - APHP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), University of Manchester [Manchester], Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPC), and Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPC)
- Subjects
030203 arthritis & rheumatology ,Muscle biopsy ,medicine.diagnostic_test ,business.industry ,Duchenne muscular dystrophy ,[SDV]Life Sciences [q-bio] ,Immunology ,Autoantibody ,medicine.disease ,3. Good health ,03 medical and health sciences ,0302 clinical medicine ,Real-time polymerase chain reaction ,Rheumatology ,Immunology and Allergy ,Medicine ,Biomarker (medicine) ,Juvenile ,business ,030217 neurology & neurosurgery ,Juvenile dermatomyositis ,Myositis ,ComputingMilieux_MISCELLANEOUS - Abstract
OBJECTIVE Juvenile idiopathic inflammatory/immune myopathies (IIMs) constitute a highly heterogeneous group of disorders with diagnostic difficulties and prognostic uncertainties. Circulating myositis-specific autoantibodies (MSAs) have been recognized as reliable tools for patient substratification. Considering the key role of type I interferon (IFN) up-regulation in juvenile IIM, we undertook the present study to investigate whether IFN-induced 15-kd protein (ISG-15) could be a reliable biomarker for stratification and diagnosis and to better elucidate its role in juvenile IIM pathophysiology. METHODS The study included 56 patients: 24 with juvenile dermatomyositis (DM), 12 with juvenile overlap myositis (OM), 10 with Duchenne muscular dystrophy, and 10 with congenital myopathies. Muscle biopsy samples were assessed by immunohistochemistry, immunoblotting, and real-time quantitative polymerase chain reaction. Negative regulators of type I IFN (ISG15 and USP18) and positive regulators of type I IFN (DDX58 and IFIH1) were analyzed. RESULTS ISG15 expression discriminated patients with juvenile IIM from those with nonimmune myopathies and, among patients with juvenile IIM, discriminated those with DM from those with OM. Among patients with juvenile DM, up-regulation of the type I IFN positive regulators DDX58 and IFIH1 was similar regardless of MSA status. In contrast, the highest levels of the type I IFN negative regulator ISG15 were observed in patients who were positive for melanoma differentiation-associated gene 5 (MDA-5). Finally, ISG15 levels were inversely correlated with the severity of muscle histologic abnormalities and positively correlated with motor performance as evaluated by the Childhood Myositis Assessment Scale and by manual muscle strength testing. CONCLUSION Muscle ISG15 expression is strongly associated with juvenile DM, with patients exhibiting a different ISG-15 muscle signature according to their MSA class. Patients with juvenile DM who are positive for MDA-5 have higher expression of ISG15 in both gene form and protein form compared to the other subgroups. Moreover, our data show that negative regulation of type I IFN correlates with milder muscle involvement.
- Published
- 2021
8. Long Term Pharmacological Perturbation of Autophagy in Mice: Are HCQ Injections a Relevant Choice?
- Author
-
Masson, Jean-Daniel, Blanchet, Benoit, Periou, Baptiste, Authier, François-Jérôme, Mograbi, Baharia, Gherardi, Romain K, and Crépeaux, Guillemette
- Subjects
dose-response ,autophagy ,hydroxychloroquine ,mice ,lcsh:Biology (General) ,long term ,lcsh:QH301-705.5 ,Article - Abstract
Macroautophagy (hereafter referred to as autophagy) is an evolutionarily conserved catabolic process whose loss-of-function has been linked to a growing list of pathologies. Knockout mouse models of key autophagy genes have been instrumental in the demonstration of the critical functions of autophagy, but they display early lethality, neurotoxicity and unwanted autophagy-independent phenotypes, limiting their applications for in vivo studies. To avoid problems encountered with autophagy-null transgenic mice, we investigated the possibility of disturbing autophagy pharmacologically in the long term. Hydroxychloroquine (HCQ) ip injections were done in juvenile and adult C57bl/6j mice, at range doses adapted from the human malaria prophylactic treatment. The impact on autophagy was assessed by western-blotting, and juvenile neurodevelopment and adult behaviours were evaluated for four months. Quite surprisingly, our results showed that HCQ treatment in conditions used in this study neither impacted autophagy in the long term in several tissues and organs nor altered neurodevelopment, adult behaviour and motor capabilities. Therefore, we recommend for future long-term in vivo studies of autophagy, to use genetic mouse models allowing conditional inhibition of selected Atg genes in appropriate lineage cells instead of HCQ treatment, until it could be successfully revisited using higher HCQ doses and/or frequencies with acceptable toxicity.
- Published
- 2020
9. Distinct interferon signatures stratify inflammatory and dysimmune myopathies
- Author
-
Rigolet, Muriel, Hou, Cyrielle, Amer, Yasmine, Aouizerate, Jessie, Periou, Baptiste, Gherardi, Romain, Lafuste, Peggy, Authier, François, Baba Amer, Yasmine, Authier, François Jérôme, Université Paris-Est Créteil Val-de-Marne - Faculté de médecine (UPEC Médecine), Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Cellules Souches, Plasticité Cellulaire, Médecine Régénératrice et Immunothérapies (IRMB), Université de Montpellier (UM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Service de néphrologie [CHU Henri Mondor], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Henri Mondor, Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Vesalius Research Center, Vesalius Research Center, VIB, Leuven, Signalisation et physiopathologie des cellules épithéliales, Université Paris-Sud - Paris 11 (UP11)-Institut National de la Santé et de la Recherche Médicale (INSERM), and Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)
- Subjects
Male ,ISG15 ,dermatomyositis ,inflammatory myopathy ,Biopsy ,[SDV]Life Sciences [q-bio] ,Gene Expression ,major histocompatibility class 2 (MHC-2) ,antisynthetase ,0302 clinical medicine ,necrotising autoimmune myopathies ,Interferon ,Immunology and Allergy ,Connective Tissue Diseases ,Myositis ,Aged, 80 and over ,medicine.diagnostic_test ,inclusion body myositis ,interferon ,Middle Aged ,3. Good health ,Female ,Disease Susceptibility ,medicine.drug ,Signal Transduction ,Adult ,Immunology ,Inflammatory myopathy ,Diagnosis, Differential ,03 medical and health sciences ,Rheumatology ,Muscular Diseases ,medicine ,CIITA ,Humans ,Muscle, Skeletal ,Aged ,030203 arthritis & rheumatology ,Muscle biopsy ,business.industry ,Dermatomyositis ,medicine.disease ,Gene Expression Regulation ,Interferons ,Inclusion body myositis ,business ,030217 neurology & neurosurgery ,CD8 ,Biomarkers ,[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology - Abstract
International audience; What is already known about this subject? ► among inflammatory/dysimmune myopathies (iDMs), dermatomyositis (DM) is the only associated with type i-interferon signature. ► Most iDMs are associated with myofiber expression of major histocompatibility complex (MHc)-class i. MHc-i is induced by interferons suggesting a possible role for type ii-interferon in iDMs other than DM. What does this study add? ► in this study, we showed that myofiber MHc-ii expression is observed in inclusion body myositis (iBM) and antisynthetase myositis (aSM), but not in DM and necrotizing autoimmune myopathy (naM). ► in accordance with this finding, we showed that iBM and aSM are specifically associated with type-ii iFnγ signature, DM only with type-i iFn signature, and naM with neither type-i nor type-ii iFn signature. How might this impact on clinical practice? ► Distinct iFn signatures allow a more distinct segregation of iDMs and therefore a more accurate diagnosis. ► Deciphering iFn signatures in iDMs will also lead to develop new therapeutic approaches targeting iFns pathways. AbstrAct Objective the role of interferons (iFn) in the pathophysiology of primary inflammatory and dysimmune myopathies (iDM) is increasingly investigated, notably because specific neutralisation approaches may constitute promising therapeutic tracks. in present work we analysed the muscular expression of specific iFnα/β and iFnγ-stimulated genes in patients with various types of iDM. Methods 39 patients with iDM with inclusion body myositis (iBM, n=9), dermatomyositis (DM, n=10), necrotising autoimmune myopathies (naM, n=10) and antisynthetase myositis (aSM, n=10), and 10 controls were included. Quantification of expression levels of iFnγ, iSg15, an iFnα/β-inducible gene and of six iFnγ-inducible genes (gBP2, Hla-DOB, Hla-DPB, ciita, Hla-DrB and Hla-DMB) was performed on muscle biopsy samples. Results DM usually associated with strong type i iFnα/β signature, iBM and aSM with prominent type ii iFnγ signature and naM with neither type i nor type ii iFn signature. immunofluorescence study in aSM and iBM showed myofibre expression of major histocompatibility class 2 (MHc-2) and ciita, confirming the induction of the iFnγ pathway. Furthermore, MHc-2-positive myofibres were observed in close proximity to cD8+ t cells which produce high levels of iFnγ. Conclusion Distinct iFn signatures allow a more distinct segregation of iDMs and myofibre MHc-2 expression is a reliable biomarker of type ii iFn signature.
- Published
- 2019
10. From Diagnosis to Prognosis: Revisiting the Meaning of Muscle ISG15 Overexpression in Juvenile Inflammatory Myopathies.
- Author
-
Hou, Cyrielle, Durrleman, Chloé, Periou, Baptiste, Barnerias, Christine, Bodemer, Christine, Desguerre, Isabelle, Quartier, Pierre, Melki, Isabelle, Rice, Gillian I., Rodero, Mathieu P., Charuel, Jean‐Luc, Relaix, Fréderic, Bader‐Meunier, Brigitte, Authier, FrançoisJérôme, and Gitiaux, Cyril
- Subjects
BIOMARKERS ,AUTOANTIBODIES ,REVERSE transcriptase polymerase chain reaction ,KRUSKAL-Wallis Test ,IMMUNOHISTOCHEMISTRY ,MANN Whitney U Test ,FISHER exact test ,GENE expression ,INTERFERONS ,T-test (Statistics) ,DESCRIPTIVE statistics ,CHI-squared test ,MYOSITIS ,POLYMERASE chain reaction ,DATA analysis software ,CARRIER proteins - Abstract
Objective: Juvenile idiopathic inflammatory/immune myopathies (IIMs) constitute a highly heterogeneous group of disorders with diagnostic difficulties and prognostic uncertainties. Circulating myositis‐specific autoantibodies (MSAs) have been recognized as reliable tools for patient substratification. Considering the key role of type I interferon (IFN) up‐regulation in juvenile IIM, we undertook the present study to investigate whether IFN‐induced 15‐kd protein (ISG‐15) could be a reliable biomarker for stratification and diagnosis and to better elucidate its role in juvenile IIM pathophysiology. Methods: The study included 56 patients: 24 with juvenile dermatomyositis (DM), 12 with juvenile overlap myositis (OM), 10 with Duchenne muscular dystrophy, and 10 with congenital myopathies. Muscle biopsy samples were assessed by immunohistochemistry, immunoblotting, and real‐time quantitative polymerase chain reaction. Negative regulators of type I IFN (ISG15 and USP18) and positive regulators of type I IFN (DDX58 and IFIH1) were analyzed. Results: ISG15 expression discriminated patients with juvenile IIM from those with nonimmune myopathies and, among patients with juvenile IIM, discriminated those with DM from those with OM. Among patients with juvenile DM, up‐regulation of the type I IFN positive regulators DDX58 and IFIH1 was similar regardless of MSA status. In contrast, the highest levels of the type I IFN negative regulator ISG15 were observed in patients who were positive for melanoma differentiation–associated gene 5 (MDA‐5). Finally, ISG15 levels were inversely correlated with the severity of muscle histologic abnormalities and positively correlated with motor performance as evaluated by the Childhood Myositis Assessment Scale and by manual muscle strength testing. Conclusion: Muscle ISG15 expression is strongly associated with juvenile DM, with patients exhibiting a different ISG‐15 muscle signature according to their MSA class. Patients with juvenile DM who are positive for MDA‐5 have higher expression of ISG15 in both gene form and protein form compared to the other subgroups. Moreover, our data show that negative regulation of type I IFN correlates with milder muscle involvement. [ABSTRACT FROM AUTHOR]
- Published
- 2021
- Full Text
- View/download PDF
11. Obesity impairs skeletal muscle repair through NID-1 mediated extracellular matrix remodeling by mesenchymal progenitors.
- Author
-
Pérez-Díaz, Sergio, Koumaiha, Zeynab, Borok, Matthew Jay, Aurade, Frederic, Pini, Maria, Periou, Baptiste, Rouault, Christine, Baba-Amer, Yasmine, Clément, Karine, Derumeaux, Genevieve, Authier, François Jérôme, Lafuste, Peggy, and Relaix, Frederic
- Subjects
- *
MYOBLASTS , *EXTRACELLULAR matrix , *SKELETAL muscle , *ADIPOSE tissues , *HOMEOSTASIS , *HIGH-fat diet , *CELL physiology , *MUSCLE regeneration - Abstract
Obesity triggers skeletal muscle physio-pathological alterations. However, the crosstalk between adipose tissue and myogenic cells remains poorly understood during obesity. We identified NID-1 among the adipose tissue secreted factors impairing myogenic potential of human myoblasts and murine muscle stem cells in vitro. Mice under High Fat Diet (HFD) displayed increased NID-1 expression in the skeletal muscle endomysium associated with intramuscular fat adipose tissue expansion and compromised muscle stem cell function. We show that NID-1 is highly secreted by skeletal muscle fibro-adipogenic/mesenchymal progenitors (FAPs) during obesity. We demonstrate that increased muscle NID-1 impairs muscle stem cells proliferation and primes the fibrogenic differentiation of FAPs, giving rise to an excessive deposition of extracellular matrix. Finally, we propose a model in which obesity leads to skeletal muscle extracellular matrix remodeling by FAPs, mediating the alteration of myogenic function by adipose tissue and highlighting the key role of NID-1 in the crosstalk between adipose tissue and skeletal muscle. A. Adult skeletal muscle mesenchymal progenitor fibro-adipogenic potential in regular diet conditions. Undifferentiated multipotent PDGFRα-expressing progenitors (FAPs) are able to generate pre-adipocytes (NID-1 low) and fibrocytes (NID-1 high) committed to become adipocytes and fibroblast-like cells, respectively, under homeostatic and regeneration condition. B. Adult MuSCs myogenic potential under regular diet. During homeostasis, MuSCs are quiescent Pax7-expressing cells. Their role is maintaining the number of skeletal muscle progenitors throughout life. However, certain stimuli, such as muscle injury, launch the muscle regeneration program. Pax7 expression is downregulated at the time MyoD is expressed. Activated myoblasts undergo several cell cycles (Ki67+) to generate abundant number of myoblasts. Following differentiation, myoblasts decrease MyoD expression, and upregulate the commitment marker MyoG. Finally, myocytes fuse to repair or generate new myotubes. C. Adult skeletal muscle mesenchymal progenitor fibro-adipogenic potential after High-Fat Diet (HFD). HFD promotes FAP infiltration into obese mouse skeletal muscle. The surplus of energy stimulates transformation of the NID-1 Low FAP subpopulation into adipocytes and therefore, intramuscular adipose tissue deposition. The overstimulation of low NID-1 expressing FAPs forces their differentiation or trans-differentiation to NID-1 high expression FAPs. In obese mice under homeostatic conditions, most FAPs are expressing high levels of NID-1 which give rise to fibroblast-like cells upon regeneration. This in turn leads to excessive extracellular matrix deposition once the muscle damage is repaired. D. Obese mice adipose tissue secretome enhances FAP's fibrogenic fate during regeneration. E. Adult MuSCs myogenic potential after HFD. The increase in NID-1 secreting-FAPs alters the MuSCs niche. In the steady state, NID-1 may maintain the quiescence of Pax7 -expressing MuSCs, giving rise to a higher number of skeletal muscle progenitors. However, upon regeneration the persistence of NID-1 may blunt MuSCs clonal expansion and favor myoblast differentiation. [Display omitted] [ABSTRACT FROM AUTHOR]
- Published
- 2022
- Full Text
- View/download PDF
12. Hemifacial myohyperplasia is due to somatic muscular PIK3CA gain-of-function mutations and responds to pharmacological inhibition.
- Author
-
Bayard C, Segna E, Taverne M, Fraissenon A, Hennocq Q, Periou B, Zerbib L, Ladraa S, Chapelle C, Hoguin C, Kaltenbach S, Villarese P, Asnafi V, Broissand C, Nemazanyy I, Autret G, Goudin N, Legendre C, Authier FJ, Viel T, Tavitian B, Gitiaux C, Fraitag S, Duong JP, Delcros C, Sergent B, Picard A, Dussiot M, Guibaud L, Khonsari R, and Canaud G
- Subjects
- Animals, Mice, Disease Models, Animal, Hypertrophy, Humans, Child, Class I Phosphatidylinositol 3-Kinases genetics, Facial Asymmetry, Gain of Function Mutation
- Abstract
Hemifacial myohyperplasia (HFMH) is a rare cause of facial asymmetry exclusively involving facial muscles. The underlying cause and the mechanism of disease progression are unknown. Here, we identified a somatic gain-of-function mutation of PIK3CA in five pediatric patients with HFMH. To understand the physiopathology of muscle hypertrophy in this context, we created a mouse model carrying specifically a PIK3CA mutation in skeletal muscles. PIK3CA gain-of-function mutation led to striated muscle cell hypertrophy, mitochondria dysfunction, and hypoglycemia with low circulating insulin levels. Alpelisib treatment, an approved PIK3CA inhibitor, was able to prevent and reduce muscle hypertrophy in the mouse model with correction of endocrine anomalies. Based on these findings, we treated the five HFMH patients. All patients demonstrated clinical, esthetical, and radiological improvement with proof of target engagement. In conclusion, we show that HFMH is due to somatic alteration of PIK3CA and is accessible to pharmacological intervention., (© 2023 Bayard et al.)
- Published
- 2023
- Full Text
- View/download PDF
13. Immunolabelling Myofiber Degeneration in Muscle Biopsies.
- Author
-
Bencze M, Periou B, Baba-Amer Y, and Authier FJ
- Subjects
- Animals, Biopsy, Cell Death, Cell Membrane metabolism, Humans, Immunoglobulins metabolism, Mice, Muscle Fibers, Skeletal metabolism, Muscle, Skeletal metabolism, Muscular Dystrophies metabolism, Necrosis, Muscle Fibers, Skeletal pathology, Muscle, Skeletal pathology, Muscular Dystrophies pathology
- Abstract
The necrosis of muscle fibres (myonecrosis) plays a central role in the pathogenesis of several muscle conditions, including muscular dystrophies. Therapeutic options addressing the causes of muscular dystrophy pathogenesis are expected to alleviate muscle degeneration. Therefore, a method to assay and quantify the extent of cell death in muscle biopsies is needed. Conventional methods to observe myofiber degeneration in situ are either poorly quantitative or rely on the injection of vital dyes. In this article, an immunofluorescence protocol is described that stains necrotic myofibers by targeting immunoglobulin G (IgG) uptake by myofibers. The IgG uptake method is based on cell features characterizing the necrotic demise, including 1) the loss of plasma membrane integrity with the release of damage-associated molecular patterns and 2) the uptake of plasmatic proteins. In murine cross-sections, the co-immunolabelling of myofibers, extracellular matrix proteins, and mouse IgG allows clean and straightforward identification of myofibers with necrotic fate. This simple method is suitable for quantitative analysis and applicable to all species, including human samples, and does not require the injection of vital dye. The staining of necrotic myofibers by IgG uptake can also be paired with other co-immunolabelling.
- Published
- 2019
- Full Text
- View/download PDF
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.