Muscle satellite cells from GRMD dystrophic dogs are not phenotypically distinguishable from wild type satellite cells in ex vivo culture

Berg, Zachary; Beffa, Lucas R.; Cook, Daniel P.; Cornelison, D.D.W.

doi:10.1016/j.nmd.2010.12.009

Cited by 14 publications

(13 citation statements)

References 36 publications

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“…When compared to cells expanded on human IgG, expanding cells on Delta-1 ext -IgG did not increase the percentage of cells expressing syndecan 4, a marker of satellite cells and satellite cell-derived myogenic cells in culture ( Figure 4B) (Table 1) [17]. In contrast, the CXCR4 receptor, which has a critical role in muscle regeneration [16], showed increased RNA and protein levels in cells expanded on Delta-1 ext -IgG ( Figure 3C and 4A), however, the percentage of CXCR4 expressing cells did not increase (Table 1), indicating a higher abundance of CXCR4 per cell.…”

Section: Activation Of Notch Signaling Inhibits Canine Myogenic Diffementioning

confidence: 98%

Activation of Notch Signaling During Ex Vivo Expansion Maintains Donor Muscle Cell Engraftment

et al. 2012

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Transplantation of myogenic stem cells possesses great potential for long-term repair of dystrophic muscle. However, a single donor muscle biopsy is unlikely to provide enough cells to effectively transplant the muscle mass of a patient affected by muscular dystrophy. Expansion of cells ex vivo using traditional culture techniques significantly reduces engraftment potential. We hypothesized that activation of Notch signaling during ex vivo expansion would maintain donor cell engraftment potential. In this study, we expanded freshly isolated canine muscle-derived cells on tissue culture plates coated with Delta-1ext-IgG to activate Notch signaling or with human IgG as a control. A model of canine-to-murine xenotransplantation was used to quantitatively compare canine muscle cell engraftment, and determine if engrafted donor cells could function as satellite cells in vivo. We show that Delta-1ext-IgG inhibited differentiation of canine muscle-derived cells, and increased the level of genes normally expressed in myogenic precursors. Moreover, cells expanded on Delta-1ext-IgG resulted in a significant increase in the number of donor-derived fibers, as compared to cells expanded on human IgG, reaching engraftment levels similar to freshly isolated cells. Importantly, cells expanded on Delta-1ext-IgG engrafted to the recipient satellite cell niche, and contributed to further regeneration. A similar strategy of expanding human muscle-derived cells on Notch ligand might facilitate engraftment and muscle regeneration for patients affected with muscular dystrophy.

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Section: Activation Of Notch Signaling Inhibits Canine Myogenic Diffementioning

confidence: 98%

Activation of Notch Signaling During Ex Vivo Expansion Maintains Donor Muscle Cell Engraftment

et al. 2012

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“…Cassano et al demonstrated that ventricle-derived CPCs from golden retriever muscular dystrophy (GRMD) dogs showed impaired self-renewal and cardiomyogenic differentiation in vitro and in vivo when compared to those from healthy dogs [53]. In comparison, a recent study showed that there were no obvious alterations to cell biology observed between satellite cells isolated from wild-type or GRMD dystrophic dogs, as determined in vitro by proliferation capacity, clonogenicity, motility, and expression of terminal differentiation proteins [54].…”

Section: Figmentioning

confidence: 99%

Murine Cardiosphere-Derived Cells Are Impaired by Age but Not by Cardiac Dystrophic Dysfunction

Hsiao

Perbellini

Gomes

et al. 2014

Stem Cells and Development

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To be clinically relevant as a therapy for heart failure, endogenous progenitor cells must be isolated and expanded from aged and/or diseased tissue. Here, we investigated the effect of age and cardiac impairment resulting from lack of dystrophin on murine cardiosphere-derived cells (CDCs). CDCs were isolated and expanded from atrial biopsies from wild-type mice aged 1.5, 6, 18, and 24 months and from mdx mice aged 6 and 18 months. Cardiac function was measured in mdx mice and age-matched wild-type mice using highresolution cine magnetic resonance imaging. CDCs could be isolated and expanded from all mice, however, the number of cells obtained, and their regenerative potential, decreased with age, as demonstrated by decreased expression of stem cell markers, c-kit and Sca-1, and decreased cell proliferation, migration, clonogenicity, and differentiation. Six-month-old mdx mice showed right ventricular (RV) dilation and reduced RV ejection fraction (EF) in comparison to wild-type mice. Older mdx mice displayed significant RV and left ventricular dilation and decreased EF in both ventricles, compared with age-matched wild-type mice. Mdx mouse hearts contained significantly more fibrotic tissue than age-matched wild-type mouse hearts. However, CDCs isolated from mice aged 6 and 18 months had the same number and regenerative potential from mdx mice and agematched wild-type mice. Thus, the cardiac progenitor cell population is impaired by age but is not substantially altered by the progressive deterioration in function of the dystrophic heart.

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“…Satellite cells from dystrophic fibers have been shown to have markedly diminished doubling times and decreased capacity for myogenic differentiation . This decline in satellite cell function may be a result of the dystrophic muscle environment, not from any intrinsic abnormalities, because a recent study found no difference between satellite cell physiology in Golden Retriever muscular dystrophy and wild‐type cells . However, this dysfunction, no matter the cause, does not allow for the usual muscle hypertrophy in response to exercise and mechanical overloading, in which there is satellite cell activation and proliferation, as well as muscle angiogenesis and release of the growth factors IGF‐1 and vascular endothelial growth factor (VEGF)…”

Section: Overview Of Exercise Studies In Nmdmentioning

confidence: 99%

Exercise in neuromuscular disease

Anziska

Sternberg

2013

Muscle and Nerve

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In this review, we present an overview of the role of exercise in neuromuscular disease (NMD). We demonstrate that despite the different pathologies in NMDs, exercise is beneficial, whether aerobic/endurance or strength/resistive training, and we explore whether this benefit has a similar mechanism to that of healthy subjects. We discuss further areas for study, incorporating imaginative and novel approaches to training and its assessment in NMD. We conclude by suggesting ways to improve future trials by avoiding previous methodological flaws and drawbacks in this field.

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Muscle satellite cells from GRMD dystrophic dogs are not phenotypically distinguishable from wild type satellite cells in ex vivo culture

Cited by 14 publications

References 36 publications

Activation of Notch Signaling During Ex Vivo Expansion Maintains Donor Muscle Cell Engraftment

Activation of Notch Signaling During Ex Vivo Expansion Maintains Donor Muscle Cell Engraftment

Murine Cardiosphere-Derived Cells Are Impaired by Age but Not by Cardiac Dystrophic Dysfunction

Exercise in neuromuscular disease

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