Histological parameters for the quantitative assessment of muscular dystrophy in the mdx-mouse

Briguet, Alexandre; Courdier-Früh, Isabelle; Foster, Mark; Meier, Thomas; Magyar, Josef P.

doi:10.1016/j.nmd.2004.06.008

Cited by 361 publications

(382 citation statements)

References 26 publications

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“…2F) and measured myofiber cross‐sectional area (CSA) and minimum Feret's diameter (MFD), which removes potential error from the sectioning process (Briguet et al ., 2004). Aging resulted in a 44% loss of CSA and a 28% loss in MFD in mice fed a control diet relative to young mice fed a control diet (Fig.…”

Section: Resultsmentioning

confidence: 99%

The histone deacetylase inhibitor butyrate improves metabolism and reduces muscle atrophy during aging

Walsh¹,

et al. 2015

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SummarySarcopenia, the loss of skeletal muscle mass and function during aging, is a major contributor to disability and frailty in the elderly. Previous studies found a protective effect of reduced histone deacetylase activity in models of neurogenic muscle atrophy. Because loss of muscle mass during aging is associated with loss of motor neuron innervation, we investigated the potential for the histone deacetylase (HDAC) inhibitor butyrate to modulate age‐related muscle loss. Consistent with previous studies, we found significant loss of hindlimb muscle mass in 26‐month‐old C57Bl/6 female mice fed a control diet. Butyrate treatment starting at 16 months of age wholly or partially protected against muscle atrophy in hindlimb muscles. Butyrate increased muscle fiber cross‐sectional area and prevented intramuscular fat accumulation in the old mice. In addition to the protective effect on muscle mass, butyrate reduced fat mass and improved glucose metabolism in 26‐month‐old mice as determined by a glucose tolerance test. Furthermore, butyrate increased markers of mitochondrial biogenesis in skeletal muscle and whole‐body oxygen consumption without affecting activity. The increase in mass in butyrate‐treated mice was not due to reduced ubiquitin‐mediated proteasomal degradation. However, butyrate reduced markers of oxidative stress and apoptosis and altered antioxidant enzyme activity. Our data is the first to show a beneficial effect of butyrate on muscle mass during aging and suggests HDACs contribute to age‐related muscle atrophy and may be effective targets for intervention in sarcopenia and age‐related metabolic disease.

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Section: Resultsmentioning

confidence: 99%

The histone deacetylase inhibitor butyrate improves metabolism and reduces muscle atrophy during aging

Walsh¹,

et al. 2015

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“…Fiber size was studied by measuring the fibers' minimal inner diameter (at least 100 fibers per muscle), defined as the minimum diameter from inner border to inner border, passing through the center of the muscle fiber. This parameter has been shown to be very insensitive to deviations from the "optimal" cross-sectioning profile, as compared with direct measure of fiber cross-sectional area (28). Cross-sectional area (CSA) was calculated using this diameter, and results were expressed as mean CSA Ϯ S.E.…”

Section: Methodsmentioning

confidence: 99%

High CO2 Levels Cause Skeletal Muscle Atrophy via AMP-activated Kinase (AMPK), FoxO3a Protein, and Muscle-specific Ring Finger Protein 1 (MuRF1)

Jaitovich

Angulo

Lecuona

et al. 2015

Journal of Biological Chemistry

104

134

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Background: CO 2 retention and skeletal muscle atrophy occur in patients with lung diseases and are associated with poor clinical outcomes. Results: Hypercapnia leads to AMPK/FoxO3a/MuRF1-dependent muscle fiber size reduction. Conclusion: Hypercapnia activates a signaling pathway leading to skeletal muscle atrophy. Significance: High CO 2 levels directly activate a proteolytic program of skeletal muscle atrophy which is of relevance to patients with lung diseases.

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“…Also, at this age there is an already described similarity of fibrosis and muscular deterioration between humans and mdx mice age-matched. See schematic Figure 1 plotted with these similarities between both species according to the literature (Briguet et al;Grounds et al, 2008;Barnabei et al, 2011;Hyzewicz et al, 2015). This research was approved by the Ethics Committee on Animal Use of the University Federal dos Vales do Jequitinhonha e Mucuri (CEUA/UFVJM), protocol number 017/2011.…”

Section: Methodsmentioning

confidence: 99%

Low Intensity Training Provokes Adaptations on Muscle Fibrosis of a Muscular Dystrophy Model

et al. 2018

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SUMMARY:Duchenne muscular dystrophy (DMD) is a genetic neuromuscular disorder with progressive clinical signs until death, around the second decade of life. Mdx is the most used animal model to pre-clinical studies of DMD. Parameters of exercise on this muscular disease are still unknown. This research aimed to investigate if the low intensity treadmill training would exacerbate the markers of muscle injury, fibrosis, and the composition of the extracellular matrix by type I and III collagens of the mdx model. Dystrophic 11-week-old male mice were separated in exercised (mdxE, n=8) and sedentary (mdxC, n=8) groups. Wild-type mice were used as control (WT, n=8). Exercised group underwent a LIT protocol (9 m/min, 30min, 3days/week, 60 days) on a horizontal treadmill. Gastrocnemius muscle was collected at day 60 and processed to morphological and morphometric analyzes. Sedentary mdx animals presented inflammatory infiltrate and necrotic fibers. Histochemical analysis revealed that the perimysium of the mdxC group is organized into thick and clustered collagen fibers, which generates a larger area of intramuscular collagen fibers for these animals. Histomorphometry attested that fraction area of collagen fibers of mdxC group was higher than mdxE group (p=0.04) and mdxE group values similar to WT group (p=1.00). Centrally located nuclei fibers and the variance coefficient (VC) of minimal Feret's diameter was similar in mdxE and mdxC groups (p=1.00) and both groups presented higher mean values than WT group (p<0.00). Immunohistochemistry revealed the presence of type I collagen mainly in the mdxC group. LIT protocol had not exacerbated muscle injuries resulting from the dystrophindeficiency membrane fragility at the same time that had reduced the intramuscular collagen deposition. LIT had positively influenced these markers of dystrophic muscle injury on gastrocnemius muscle of mdx model.

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Histological parameters for the quantitative assessment of muscular dystrophy in the mdx-mouse

Cited by 361 publications

References 26 publications

The histone deacetylase inhibitor butyrate improves metabolism and reduces muscle atrophy during aging

The histone deacetylase inhibitor butyrate improves metabolism and reduces muscle atrophy during aging

High CO2 Levels Cause Skeletal Muscle Atrophy via AMP-activated Kinase (AMPK), FoxO3a Protein, and Muscle-specific Ring Finger Protein 1 (MuRF1)

Low Intensity Training Provokes Adaptations on Muscle Fibrosis of a Muscular Dystrophy Model

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