Satellite cell depletion in degenerative skeletal muscle

Jejurikar, Sameer S.; Kuzon, William M.

doi:10.1023/a:1026127307457

Cited by 125 publications

(112 citation statements)

References 69 publications

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“…In this context, satellite cells and their response to stress such as oxidative stress are important to mature skeletal muscle performance and function. Of significance for our work, enhanced satellite cell apoptosis has been related to compromised recovery potential in skeletal muscle of aged animals ( Jejurikar & Kuzon 2003, Jejurikar et al 2006.…”

Section: Discussionmentioning

confidence: 98%

“…C2C12 cells resemble these activated satellite cells. Moreover, apoptosis increases significantly with age affecting satellite cells and contributing to sarcopenia ( Jejurikar & Kuzon 2003). Therefore, knowledge of the mechanism underlying the antiapoptotic action of E 2 in C2C12 myoblasts is relevant to understand the hormone protective effects on satellite skeletal cells.…”

Section: Introductionmentioning

confidence: 99%

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Estradiol exerts antiapoptotic effects in skeletal myoblasts via mitochondrial PTP and MnSOD

Colla¹,

Vasconsuelo²,

Boland³

2012

Journal of Endocrinology

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Abstract17b-Estradiol (E 2 ) protects several non-reproductive tissues from apoptosis, including skeletal muscle. We have shown that E 2 at physiological concentrations prevented apoptosis induced by H 2 O 2 in C2C12 skeletal myoblasts. As we also demonstrated the presence of estrogen receptors in mitochondria, the present work was focused on the effects of E 2 on this organelle. Specifically, we evaluated the actions of E 2 on the mitochondrial permeability transition pore (MPTP) by the calcein-acetoxymethylester/cobalt method using fluorescence microscopy and flow cytometry. Pretreatment with E 2 prevented MPTP opening induced by H 2 O 2 , which preceded loss of mitochondrial membrane potential. In addition, it was observed that H 2 O 2 induced translocation of Bax to mitochondria; however, in the presence of the steroid this effect was abrogated suggesting that members of the Bcl-2 family may be regulated by E 2 to exert an antiapoptotic effect. Moreover, E 2 increased mitochondrial manganese superoxide dismutase protein expression and activity, as part of a mechanism activated by E 2 that improved mitochondrial performance. Our results suggest a role of E 2 in the regulation of apoptosis with a clear action at the mitochondrial level in C2C12 skeletal myoblast cells. Key Words" 17b-estradiol " C2C12 skeletal myoblasts

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Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Estradiol exerts antiapoptotic effects in skeletal myoblasts via mitochondrial PTP and MnSOD

Colla¹,

Vasconsuelo²,

Boland³

2012

Journal of Endocrinology

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“…Evaluation of H&E-stained sections was carried out on the tibialis anterior and diaphragm muscles. The muscle obtained from untreated ␣-SG-null mice revealed a progressive degeneration, with the appearance of necrotic and calcified fibers, which was accompanied by an increase in centronucleated, regenerating fibers early on, followed by a decrease, most likely because of depletion of satellite cells (22) (Fig. 2 A and B).…”

Section: Hct 1026 Enhances Regeneration and Protects Skeletal Muscle Inmentioning

confidence: 97%

Nitric oxide release combined with nonsteroidal antiinflammatory activity prevents muscular dystrophy pathology and enhances stem cell therapy

Brunelli

Sciorati

D’Antona

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

148

160

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Duchenne muscular dystrophy is a relatively common disease that affects skeletal muscle, leading to progressive paralysis and death. There is currently no resolutive therapy. We have developed a treatment in which we combined the effects of nitric oxide with nonsteroidal antiinflammatory activity by using HCT 1026, a nitric oxide-releasing derivative of flurbiprofen. Here, we report the results of long-term (1-year) oral treatment with HCT 1026 of two murine models for limb girdle and Duchenne muscular dystrophies (␣-sarcoglycan-null and mdx mice). In both models, HCT 1026 significantly ameliorated the morphological, biochemical, and functional phenotype in the absence of secondary effects, efficiently slowing down disease progression. HCT 1026 acted by reducing inflammation, preventing muscle damage, and preserving the number and function of satellite cells. HCT 1026 was significantly more effective than the corticosteroid prednisolone, which was analyzed in parallel. As an additional beneficial effect, HCT 1026 enhanced the therapeutic efficacy of arterially delivered donor stem cells, by increasing 4-fold their ability to migrate and reconstitute muscle fibers. The therapeutic strategy we propose is not selective for a subset of mutations; it provides ground for immediate clinical experimentation with HCT 1026 alone, which is approved for use in humans; and it sets the stage for combined therapies with donor or autologous, genetically corrected stem cells.HCT 1026 ͉ satellite cells ͉ skeletal muscle ͉ ␣-sarcoglycan-null mice ͉ mdx mice

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“…3,4,[7][8][9][10] Impaired activity of muscle progenitor or satellite cells also might contribute to CKD-induced muscle atrophy as it does in other catabolic conditions. 11,12 Satellite cells are located beneath the basal lamina of myofibers and have at least two functions. First, they proliferate, becoming myoblasts, and then differentiate, forming new muscle fibers to repair injured muscle.…”

mentioning

confidence: 99%

“…9 In mice with muscle atrophy from hindlimb suspension or in rodent models of aging, myopathy, or muscle denervation, the number and activity of satellite cells were found to be reduced, indicating that satellite cells are involved in maintaining muscle mass. 11,12 After muscle injury, satellite cells are activated and express the MyoD and myogenin transcription factors, leading to cell proliferation and differentiation, respectively. 14 -16 When these cells express embryonic myosin heavy-chain protein (eMyHC), there is myotube formation.…”

mentioning

confidence: 99%

Satellite Cell Dysfunction and Impaired IGF-1 Signaling Cause CKD-Induced Muscle Atrophy

Zhang

Wang

Wang³

et al. 2010

Journal of the American Society of Nephrology

183

216

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Muscle wasting in chronic kidney disease (CKD) begins with impaired insulin/IGF-1 signaling, causing abnormal protein metabolism. In certain models of muscle atrophy, reduced satellite cell function contributes to atrophy, but how CKD affects satellite cell function is unknown. Here, we found that isolated satellite cells from mice with CKD had less MyoD, the master switch of satellite cell activation, and suppressed myotube formation compared with control mice. In vivo, CKD delayed the regeneration of injured muscle and decreased MyoD and myogenin expression, suggesting that CKD impairs proliferation and differentiation of satellite cells. In isolated satellite cells from control mice, IGF-1 increased the expression of myogenic genes through an Akt-dependent pathway. CKD impaired Akt phosphorylation in satellite cells after muscle injury. To test whether impaired IGF-1 signaling could be responsible for decreased satellite cell function in CKD, we created an inducible IGF-1 receptor knockout mouse and found impaired satellite cell function and muscle regeneration. In addition, both CKD and IGF-1 receptor knockout mice developed fibrosis in regenerating muscles. Taken together, impaired IGF-1 signaling in CKD not only leads to abnormal protein metabolism in muscle but also impairs satellite cell function and promotes fibrosis in regenerating muscle. These signaling pathways may hold potential therapeutic targets to reduce CKD-related muscle wasting.

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Satellite cell depletion in degenerative skeletal muscle

Cited by 125 publications

References 69 publications

Estradiol exerts antiapoptotic effects in skeletal myoblasts via mitochondrial PTP and MnSOD

Estradiol exerts antiapoptotic effects in skeletal myoblasts via mitochondrial PTP and MnSOD

Nitric oxide release combined with nonsteroidal antiinflammatory activity prevents muscular dystrophy pathology and enhances stem cell therapy

Satellite Cell Dysfunction and Impaired IGF-1 Signaling Cause CKD-Induced Muscle Atrophy

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