Dystrophy and myogenesis inmdx diaphragm muscle

Anderson, Judy E.; Garrett, Kerryn L.; Moor, Andrea N.; McIntosh, Laura; Penner, Kristen M.

doi:10.1002/(sici)1097-4598(199809)21:9<1153::aid-mus6>3.0.co;2-6

Cited by 41 publications

(36 citation statements)

References 64 publications

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“…Differences in satellite cell proliferative capacity have also been reported among different adult skeletal muscles (38). To our knowledge, only one study has examined the proliferative capacity of mdx diaphragm satellite cells, and it reported no statistically significant defects of proliferation in vitro (3). However, the possibility that satellite cell function or other aspects of muscle repair are defective in the intact diaphragm of mdx mice in vivo cannot be excluded on this basis alone.…”

mentioning

confidence: 73%

“…The muscle was removed from the bath, and Lo was directly measured under a dissecting microscope with calipers accurate to 0.1 mm. Total muscle strip cross-sectional area was determined by dividing muscle weight by its length and tissue density (1.056 g/cm 3 ). This allowed diaphrag-matic-specific force to be calculated, which was expressed as newtons per square centimeter.…”

Section: Physiological Evaluation Of Diaphragmatic Injury and Repairmentioning

confidence: 85%

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Regenerative capacity of the dystrophic (mdx) diaphragm after induced injury

Matecki

Guibinga

Petrof

2004

American Journal of Physiology-Regulatory, Integrative and Comp

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mentioning

confidence: 73%

Section: Physiological Evaluation Of Diaphragmatic Injury and Repairmentioning

confidence: 85%

Regenerative capacity of the dystrophic (mdx) diaphragm after induced injury

Matecki

Guibinga

Petrof

2004

American Journal of Physiology-Regulatory, Integrative and Comp

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“…To test for regional differences within the costal diaphragm and between the costal and crural diaphragm and psoas, ANOVA was used. To determine group differences in collagen cross-sectional areas, 15 fields from each subject were pooled [15] for analysis by group and region. For significant main effects, Tukey's post hoc test was used.…”

Section: Discussionmentioning

confidence: 99%

Increased injury and intramuscular collagen of the diaphragm in COPD: autopsy observations

Scott

Wang²,

Road³

et al. 2006

Eur Respir J

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Evidence for diaphragm injury in people with chronic obstructive pulmonary disease (COPD) has been reported, although the extent of injury and collagen accumulation post mortem have not previously been examined. In addition, it is not known whether the amount of injury and collagen are different in key regions of the diaphragm.The cross-sectional area of collagen and the percentage of abnormal myofibres in the post mortem diaphragm and psoas major were determined by computer-assisted image analysis of stained cross-sections of the diaphragm for collagen with picrosirius red and with haematoxylin and eosin for morphology.In the midcostal diaphragm of six subjects with COPD and six subjects with no significant respiratory disease, the COPD diaphragm displayed a greater cross-sectional area of collagen and percentage of abnormal myofibres (collagen: 24.2¡1.0 versus 18.6¡1.1%; injury: 28.4¡7.2 versus 12.0¡1.3%). In 18 patients with various respiratory conditions, the midcostal diaphragm displayed more collagen and abnormal myofibres than the crural diaphragm, while both costal and crural diaphragms displaying more collagen and abnormal myofibres than psoas major.This study reveals extensive injury and collagen accumulation in the chronic obstructive pulmonary diseased diaphragm, and reveals a regional pattern of injury and intramuscular collagen which may correspond to variations in diaphragm loading.

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“…Only diaphragm muscles were used for analysis in this study. We dissected diaphragms rapidly from mice after opening the anterior abdominal wall at the midline and cutting "flaps" laterally to both sides from the midline; the central tendon was gripped in forceps, and scissors were used to cut quickly around the perimeter of the muscle at anterior and posterior costal and lumbar attachments (5). Diaphragms from four groups (C, P, M, MϩP) were photographed for later macroscopic assessment.…”

Section: Methodsmentioning

confidence: 99%

Nitric oxide donors improve prednisone effects on muscular dystrophy in the mdx mouse diaphragm

Mizunoya¹,

Upadhaya²,

Burczynski

et al. 2011

American Journal of Physiology-Cell Physiology

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Mizunoya W, Upadhaya R, Burczynski FJ, Wang G, Anderson JE. Nitric oxide donors improve prednisone effects on muscular dystrophy in the mdx mouse diaphragm. Am J Physiol Cell Physiol 300: C1065-C1077, 2011. First published January 26, 2011 doi:10.1152/ajpcell.00482.2010.-In Duchenne muscular dystrophy (DMD), palliative glucocorticoid therapy can produce myopathy or calcification. Since increased nitric oxide synthase activity in dystrophic mice promotes regeneration, the outcome of two nitric oxide (NO) donor drugs, MyoNovin (M) and isosorbide dinitrate (I), on the effectiveness of the anti-inflammatory drug prednisone (P) in alleviating progression of dystrophy was tested. Dystrophic mdx mice were treated (18 days) as controls or with an NO donor Ϯ P. Fiber permeability and DNA synthesis were labeled by Evans blue dye (EBD) and bromodeoxyuridine uptake, respectively. P decreased body weight gain, M increased quadriceps mass, and I increased heart mass. P increased fiber permeability (%EBDϩ fibers) and calcification in diaphragm. Treatment with NO donors ϩ P (MϩP, IϩP) reduced %EBDϩ fibers and calcification vs. P alone. %EBDϩ fibers in MϩP diaphragm did not differ from control. NO donor treatment reduced proliferation and the population of c-metϩ cells and accelerated fiber regeneration. Concurrent with P, NO donor treatment suppressed two important detrimental effects of P in mice, possibly by accelerating regeneration, rebalancing satellite cell quiescence and activation in dystrophy, and/or increasing perfusion. Results suggest that NO donors could improve current therapy for DMD.Duchenne muscular dystrophy; skeletal muscle; satellite cells; glucocorticoid MUSCULAR DYSTROPHIES are lethal genetic muscle diseases, and the most common form, Duchenne muscular dystrophy (DMD), is caused by mutation in the dystrophin gene (37). Absence of dystrophin from the cytoskeleton in DMD fibers leads to disruption of the sarcolemma by mechanical stress or exercise and progressive muscle weakness and wasting (20,27,56,69). Investigations of possible therapeutic interventions using the mdx mouse model of DMD have examined gene therapy by viral delivery of full-length dystrophin (28) or microdystrophin (97), stem (satellite) cell transplantation (40), and read-through (91) or exon-skipping approaches (2, 55, 93) to restore dystrophin expression. As these investigations are ongoing, pharmacological treatment with glucocorticoids remains the current "gold standard" therapy in DMD.Treatment with prednisone promotes a palliative reduction in inflammation and delays disease progression (57, 58) in DMD. In DMD patients and mdx mice, prednisone and deflazacort reduce the secondary inflammation that extends muscle fiber necrosis outside the region of primary damage that is caused by exercise-induced membrane breaks or eccentric contraction (25, 63). In addition, deflazacort also upregulates the calcineurin/nuclear factor of activated T cells (NFAT) pathway activity, which counteracts the muscle-specific activation of JNK1 that damages...

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Dystrophy and myogenesis inmdx diaphragm muscle

Cited by 41 publications

References 64 publications

Regenerative capacity of the dystrophic (mdx) diaphragm after induced injury

Regenerative capacity of the dystrophic (mdx) diaphragm after induced injury

Increased injury and intramuscular collagen of the diaphragm in COPD: autopsy observations

Nitric oxide donors improve prednisone effects on muscular dystrophy in the mdx mouse diaphragm

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