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Rouger, K.

Publications and source records attributed to Rouger, K..

4 recordsLinked to original sources

Super-resolution imaging with deep learning-based segmentation for detailed characterization of mitochondrial arrangement in Pompe disease skeletal muscle

Pompe disease (glycogen storage disease type II) is an autosomal recessive lysosomal storage disorder caused by acid -glucosidase deficiency, leading to lysosomal glycogen accumulation, autophagosome buildup, and defective autophagic flux. Mitochondrial abnormalities, traditionally described by electron microscopy as paracrystalline inclusions, cristae loss, and swollen structures, have long been considered secondary consequences of lysosomal dysfunction. However, the spatial organization, organelle crosstalk, and fiber-type-specific progression of these alterations in skeletal muscle remain poorly understood. We combined super-resolution image scanning microscopy with deep learning-based segmentation to quantitatively assess mitochondrial and lysosomal remodeling, and their direct physical interactions, in Pompe disease (Gaa-/-) mice. Organelles were analyzed at pre-symptomatic (1 month) and symptomatic (4 months) stages across different muscle types (Soleus, Gastrocnemius), fiber types, and subcellular regions (subsarcolemmal, intermyofibrillar). Mitochondrial network structure was altered as early as 1 month of age, whereas density changes became widespread at 4 months in a fiber-type- and region-dependent manner. Alongside early lysosomal enlargement and late-stage spatial clustering, we observed a progressive, region-specific increase in mitochondria-lysosome contacts, most pronounced in the intermyofibrillar region. This quantitative framework provides a powerful tool for monitoring pathophysiology and evaluating therapeutic interventions in Pompe disease.

pathology↗

Declining muscle hyperplasia in juvenile trout is driven by rapid limitation of muscle stem cell capacity and niche functionality

Unlike mammals and birds, where new muscle fiber formation (hyperplasia) ceases around birth, large and fast-growing fish such as rainbow trout undergo a spectacular post-hatching surge of hyperplasia, followed by a considerably delayed hyperplasia decline. This study investigated the roles of the satellite cells (SCs) and their niche in this decline by determining the number and the myogenic capacity of the muscle progenitors as well as the functionality of their direct tissue environment. Histological analysis revealed a significant decrease in hyperplasia (fibers <25 {micro}m) and SC numbers (Pax7+) between 10 g and 500 g trout. Transplantation experiments using muscle-derived cells (MDCs) from mlc2-GFP transgenic trout (10 g to 2 kg donors into 10 g to 2 kg recipients) demonstrated a marked decline in both intrinsic myogenic capacity and niche functionality as trout grow from 10 g to 500 g. Detailed analyses of GFP+ fibers produced after transplantation showed an enrichment of small-diameter GFP+ fibers in 10 g but not 100 g trout recipient muscles, showing a rapid impairment in niche ability to support hyperplasia. In addition, transplantation of MDCs from trout of different ages but the same weight, showed that increasing trout weight, but not aging, is associated with an impairment of the myogenic capacity of progenitors and their niche. Overall, these findings show that the muscle hyperplasia decline in trout is primarily driven by early impairment of the SC niche, followed by a reduction in their myogenic capacity and number, with weight gain playing a more critical role than aging.

cell biology↗

Distinct muscle stem cell fates governing hyperplasia and hypertrophy muscle growth in fish

BackgroundIn vertebrates, skeletal muscle grows postnatally through different strategies. While mammals predominantly rely on fiber hypertrophy after birth, many teleost fish retain the unique ability to generate new fibers via hyperplasia well into juvenile stages. The molecular mechanisms linked to the transition between hyperplastic-hypertrophic and hypertrophic muscle growth modes in fish remain poorly understood. ResultsWe generated a single-cell transcriptomic atlas of muscle-derived cells from juvenile Oncorhynchus mykiss (rainbow trout) at five growth stages. Fifteen tissue resident cell populations were identified, including eight myogenic subpopulations spanning from quiescent stem cells to terminally differentiating myocytes. Two distinct transcriptional trajectories were uncovered thanks to RNA velocity analysis: one present only during hyperplastic growth and another maintained throughout growth, raising the possibility of specialization of muscle stem cells toward hyperplasia or hypertrophy. Comparative analyses with human single-cell atlases suggest that some trout myogenic subpopulations correlated with hyperplastic or hypertrophic muscle growth share similarities with human stage-specific (fetal or adult) myogenic subpopulations. Strikingly, we identified a population of pax7+/pdgfr+ cells, indicating plasticity toward fibroblastic lineage and associating these cells with hypertrophic growth. Furthermore, both intrinsic changes in muscle stem cells and extrinsic remodeling of the extracellular matrix accompanied the skeletal muscle growth, suggesting a dynamic crosstalk between myogenic and mesenchymal compartments. ConclusionsOur findings reveal the existence of two transcriptionally distinct muscle stem cell fates that correlate with hyperplastic and hypertrophic muscle growth in trout. The identification of a tissue-resident pax7+/pdgfr+ subpopulation provides new insights into muscle stem cell plasticity and niche remodeling. This work establishes a comparative framework to explore the regulation of postnatal muscle growth across vertebrates.

cell biology↗

Immunological characterization of a rat model of Duchenne’s disease and demonstration of improved muscle strength after anti-CD45RC antibody treatment

Duchenne muscular dystrophy (DMD) has as standard pharmacological therapy with corticoisteroids (CS) that decrease inflammation and immune responses present in patients and animal models. CS have however limited efficacy and important and numerous side effects. Therefore, there is a need for new anti-inflammatory and pro-tolerogenic treatments that could replace or decrease doses of CS. We first assessed the status of immune system of dystrophin-deficient rats (Dmdmdx) that closely reproduce the phenotype of DMD patients. Dmdmdx rats showed increased leukocyte infiltration in skeletal and cardiac muscles, containing mostly macrophages but also T cells, and increased expression of several cytokines. Anti-CD45RC Monoclonal antibody (Mab) treatment induced immune tolerance in models of organ transplantation and GVHD (Graft Versus Host Disease). We observed that muscles and blood of DMD patients contained T CD4+ and CD8+ expressing high levels of CD45RChigh cells. Treatment of young Dmdmdx rats with anti-CD45RC MAb corrected skeletal muscle strength associated to a depletion of effectors CD45RChigh T cells with no obvious side-effects. Prednisolone treatment of Dmdmdx rats similarly increased skeletal muscle strength and was also associated to a depletion of effectors CD45RChigh cells but resulted in severe weight loss.\n\nOverall, Dmdmdx rats display important immune inflammatory response and thus represent a useful model to analyze new anti-inflammatory and tolerogenic treatments for DMD. As an example, a new treatment with anti-CD45RC antibodies improved muscle strength in Dmdmdx rats as prednisolone did but without side effects. Anti-CD45RC therapy could complement other therapies in DMD patients.

immunology↗