The Radiosensitivity of Satellite Cells: Cell Cycle Regulation, Apoptosis and Oxidative Stress

Caiozzo, Vincent J.; Giedzinski, Erich; Baker, Mike; Suárez, Tatiana; Izadi, Atefeh; Lan, Mary L.; Cho-Lim, J.J.; Tseng, Bertrand P.; Limoli, Charles L.

doi:10.1667/rr2190.1

Cited by 37 publications

(24 citation statements)

References 38 publications

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“…As noted above, we recently observed that γ radiation reduces NO levels in satellite cells (20). This observation combined with those of Anderson (21) and Allen and colleagues (22–25, 31–33) suggests that the impaired proliferation in irradiated satellite cells might be amenable to rescue by manipulation of NO levels through pharmacological or mechanotransduced interventions.…”

Section: Discussionsupporting

confidence: 52%

“…Unlike these overt forms of injury, irradiation of skeletal muscle elicits more subtle effects that can impair the impressive regenerative capacity of skeletal muscle by adversely impacting the activation and proliferation of satellite cells. In this context, we observed previously (20) that clinically relevant doses of γ radiation produced significant reductions in satellite cell proliferation. We also observed that γ radiation of satellite cells produced a reduction in their NO levels.…”

Section: Discussionmentioning

confidence: 68%

“…We performed a series of baseline studies in a previous study (20) in which we examined the effects of clinical doses of γ radiation on satellite cell proliferation, cell cycle regulation, DNA double-strand breaks, oxidative stress and NO levels. The effect of γ radiation on satellite cell NO levels was of particular interest because Anderson (21) and Allen and colleagues (22–24) demonstrated that the proliferation of satellite cells was dependent on elevations in NO, acting through an MMP2/HGF/c-met-mediated pathway.…”

Section: Introductionmentioning

confidence: 99%

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Satellite Cells Say NO to Radiation

et al. 2011

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Skeletal muscles are commonly exposed to radiation for diagnostic procedures and the treatment of cancers and heterotopic bone formation. Few studies have considered the impact of clinical doses of radiation on the ability of satellite cells (myogenic stem cells) to proliferate, differentiate and contribute to recovering/maintaining muscle mass. The primary objective of this study was to determine whether the proliferation of irradiated satellite cells could be rescued by manipulating NO levels via pharmacological approaches and mechanical stretch (which is known to increase NO levels). We used both SNP (NO donor) and PTIO (NO scavenger) to manipulate NO levels in satellite cells. We observed that SNP was highly effective in rescuing the proliferation of irradiated satellite cells, especially at doses less than 5 Gy. The potential importance of NO was further illustrated by the effects of PTIO, which completely inhibited the rescue effect of SNP. Mechanical cyclic stretch was found to produce significant increases in NO levels of irradiated satellite cells, and this was associated with a robust increase in satellite cell proliferation. The effects of both radiation and NO on two key myogenic regulatory factors (MyoD and myogenin) were also explored. Irradiation of satellite cells produced a significant increase in both MyoD and myogenin, effects that were mitigated by manipulating NO levels via SNP. Given the central role of myogenic regulatory factors in the proliferation and differentiation of satellite cells, the findings of the current study underscore the need to more fully understand the relationship between radiation, NO and the functionality of satellite cells.

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Section: Discussionsupporting

confidence: 52%

Section: Discussionmentioning

confidence: 68%

Section: Introductionmentioning

confidence: 99%

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Satellite Cells Say NO to Radiation

et al. 2011

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“…However, acutely, radiation prevents mitosis of progenitor myosatellite cells (16), disrupts cell membrane permeability and lipid fluidity, and can result in sodium-potassium pump failure at the neuromuscular junction (17). Additionally, in the long-term, post-radiation inflammation, mediated by the transforming growth factor-β family, may prevent muscle growth (18), radiation-induced vascular and parenchymal damage may interfere with muscle nutrition (19), and mantle radiation may result in nemaline myopathy (20), potentially contributing to muscular atrophy (21–26), fibrosis (25–27), and hypoplasia (28).…”

Section: Resultsmentioning

confidence: 99%

A Systematic Review of Selected Musculoskeletal Late Effects in Survivors of Childhood Cancer

Gawade¹,

Hudson²,

Kaste³

et al. 2015

CPR

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Survivors of childhood cancer are at risk for treatment-related musculoskeletal late effects. Early detection and orthopedic intervention can help ameliorate musculoskeletal late effects and prevent subsequent complications. This systematic review summarizes the literature describing associations between cancer, its treatment, and musculoskeletal late effects. We searched PubMed and Web of Science for English language articles published between January 1970 and December 2012. The search was limited to investigations with at least 15 participants and conducted at least 2 years after completion of therapy for childhood, adolescent, or young adult cancer. Some late skeletal effects, including low bone mineral density, osteonecrosis, slipped capital femoral epiphyses, oncogenic rickets, and hormone-related growth disturbances have been previously reviewed and were excluded, as were outcomes following amputation and limb-salvage procedures. Of 2347 references identified, 30 met inclusion criteria and were retained. An additional 54 studies that met inclusion criteria were found in reference lists of retained studies. Of 84 studies, 60 focused on associations between radiotherapy, six between chemotherapy, and 18 between surgery and musculoskeletal late effects. We found that younger age, higher radiation dosage, and asymmetric or partial bone radiation volume influences the effects of radiation on the musculoskeletal system. Methotrexate and vincristine are associated with long-term muscular strength and flexibility deficits. Laminectomy and chest wall resection are associated with spinal malalignment, and enucleation is associated with orbital deformities among survivors. Radiotherapy, chemotherapy, and surgery are associated with musculoskeletal late effects independently and additively. Associations are additionally influenced by host and treatment characteristics.

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“…Despite the potential benefits of fractionation, lower radiation doses that are more clinically relevant can also impair skeletal muscle development26 and increase indices of muscle remodeling 27. Altered muscle plasticity following radiation exposure has been attributed to impaired satellite cell activity 26,28,29. Satellite cell and myoblast proliferation are reduced with as little as 2 Gy radiation exposure 28–30.…”

Section: Introductionmentioning

confidence: 99%

The effect of radiation dose on mouse skeletal muscle remodeling

Hardee

Puppa

Fix

et al. 2014

Radiology and Oncology

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BackgroundThe purpose of this study was to determine the effect of two clinically relevant radiation doses on the susceptibility of mouse skeletal muscle to remodeling.Materials and methods.Alterations in muscle morphology and regulatory signaling were examined in tibialis anterior and gastrocnemius muscles after radiation doses that differed in total biological effective dose (BED). Female C57BL/6 (8-wk) mice were randomly assigned to non-irradiated control, four fractionated doses of 4 Gy (4x4 Gy; BED 37 Gy), or a single 16 Gy dose (16 Gy; BED 100 Gy). Mice were sacrificed 2 weeks after the initial radiation exposure.ResultsThe 16 Gy, but not 4x4 Gy, decreased total muscle protein and RNA content. Related to muscle regeneration, both 16 Gy and 4x4 Gy increased the incidence of central nuclei containing myofibers, but only 16 Gy increased the extracellular matrix volume. However, only 4x4 Gy increased muscle 4-hydroxynonenal expression. While both 16 Gy and 4x4 Gy decreased IIB myofiber mean cross-sectional area (CSA), only 16 Gy decreased IIA myofiber CSA. 16 Gy increased the incidence of small diameter IIA and IIB myofibers, while 4x4 Gy only increased the incidence of small diameter IIB myofibers. Both treatments decreased the frequency and CSA of low succinate dehydrogenase activity (SDH) fibers. Only 16 Gy increased the incidence of small diameter myofibers having high SDH activity. Neither treatment altered muscle signaling related to protein turnover or oxidative metabolism.ConclusionsCollectively, these results demonstrate that radiation dose differentially affects muscle remodeling, and these effects appear to be related to fiber type and oxidative metabolism.

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The Radiosensitivity of Satellite Cells: Cell Cycle Regulation, Apoptosis and Oxidative Stress

Cited by 37 publications

References 38 publications

Satellite Cells Say NO to Radiation

Satellite Cells Say NO to Radiation

A Systematic Review of Selected Musculoskeletal Late Effects in Survivors of Childhood Cancer

The effect of radiation dose on mouse skeletal muscle remodeling

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