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  • 1
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    Online Resource
    Estrogen Regulates the Satellite Cell Compartment in Females
    Elsevier BV ; 2019
    In:  Cell Reports Vol. 28, No. 2 ( 2019-07), p. 368-381.e6
    Details
    In: Cell Reports, Elsevier BV, Vol. 28, No. 2 ( 2019-07), p. 368-381.e6
    Type of Medium: Online Resource
    ISSN: 2211-1247
    URL: Article
    DOI: 10.1016/j.celrep.2019.06.025
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2019
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  • 2
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    Estradiol deficiency reduces the satellite cell pool by impairing cell cycle progression
    American Physiological Society ; 2022
    In:  American Journal of Physiology-Cell Physiology Vol. 322, No. 6 ( 2022-06-01), p. C1123-C1137
    Details
    In: American Journal of Physiology-Cell Physiology, American Physiological Society, Vol. 322, No. 6 ( 2022-06-01), p. C1123-C1137
    Abstract: The size of the satellite cell pool is reduced in estradiol (E 2 )-deficient female mice and humans. Here, we use a combination of in vivo and in vitro approaches to identify mechanisms, whereby E 2 deficiency impairs satellite cell maintenance. By measuring satellite cell numbers in mice at several early time points postovariectomy (Ovx), we determine that satellite cell numbers decline by 33% between 10 and 14 days post-Ovx in tibialis anterior and gastrocnemius muscles. At 14 days post-Ovx, we demonstrate that satellite cells have a reduced propensity to transition from G 0 /G 1 to S and G 2 /M phases, compared with cells from ovary-intact mice, associated with changes in two key satellite cell cycle regulators, ccna2 and p16 INK4a . Further, freshly isolated satellite cells treated with E 2 in vitro have 62% greater cell proliferation and require less time to complete the first division. Using clonal and differentiation assays, we measured 69% larger satellite cell colonies and enhanced satellite cell-derived myoblast differentiation with E 2 treatment compared with vehicle-treated cells. Together, these results identify a novel mechanism for preservation of the satellite cell pool by E 2 via promotion of satellite cell cycling.
    Type of Medium: Online Resource
    ISSN: 0363-6143 , 1522-1563
    URL: Article
    DOI: 10.1152/ajpcell.00429.2021
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2022
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  • 3
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    Oestradiol affects skeletal muscle mass, strength and satellite cells following repeated injuries
    Wiley ; 2020
    In:  Experimental Physiology Vol. 105, No. 10 ( 2020-10), p. 1700-1707
    Details
    In: Experimental Physiology, Wiley, Vol. 105, No. 10 ( 2020-10), p. 1700-1707
    Abstract: What is the central question of this study? Oestradiol (E 2 ) plays an important role in regulating skeletal muscle strength in females. To what extent does E 2 deficiency affect recovery of strength and satellite cell number when muscle is challenged by multiple injuries? What is the main finding and its importance? E 2 deficiency impairs the adaptive potential of skeletal muscle following repeated injuries, as measured by muscle mass and strength. The impairment is likely multifactorial with our data indicating that one mechanism is reduction in satellite cell number. Our findings have implications for ageing, hormone replacement and regenerative medicine in regards to maintaining satellite cell number and ultimately the preservation of skeletal muscle's adaptive potential. Abstract Oestradiol's effects on skeletal muscle are multifactorial including the preservation of mass, contractility and regeneration. Here, we aimed to determine the extent to which oestradiol deficiency affects strength recovery when muscle is challenged by multiple BaCl 2 ‐induced injuries and to assess how satellite cell number is influenced by the combination of oestradiol deficiency and repetitive skeletal muscle injuries. A longitudinal study was designed, using an in vivo anaesthetized mouse approach to precisely and repeatedly measure maximal isometric torque, coupled with endpoint fluorescence‐activated cell sorting to quantify satellite cells. Isometric torque and strength gains were lower in ovariectomized mice at several time points after the injuries compared to those treated with 17β‐oestradiol. Satellite cell number was 41–43% lower in placebo‐ than in oestradiol‐treated ovariectomized mice, regardless of injury status or number of injuries. Together, these results indicate that the loss of oestradiol blunts adaptive strength gains and that the number of satellite cells likely contributes to the impairment.
    Type of Medium: Online Resource
    ISSN: 0958-0670 , 1469-445X
    URL: Issue
    URL: Article
    DOI: 10.1113/eph.v105.10
    DOI: 10.1113/EP088827
    Language: English
    Publisher: Wiley
    Publication Date: 2020
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  • 4
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    Tetrahydrobiopterin synthesis and metabolism is impaired in dystrophin‐deficient mdx mice and humans
    Wiley ; 2021
    In:  Acta Physiologica Vol. 231, No. 4 ( 2021-04)
    Details
    In: Acta Physiologica, Wiley, Vol. 231, No. 4 ( 2021-04)
    Abstract: Loss of dystrophin causes oxidative stress and affects nitric oxide synthase‐mediated vascular function in striated muscle. Because tetrahydrobiopterin is an antioxidant and co‐factor for nitric oxide synthase, we tested the hypothesis that tetrahydrobiopterin would be low in mdx mice and humans deficient for dystrophin. Methods Tetrahydrobiopterin and its metabolites were measured at rest and in response to exercise in Duchenne and Becker muscular dystrophy patients, age‐matched male controls as well as wild‐type, mdx and mdx mice transgenically overexpressing skeletal muscle‐specific dystrophins. Mdx mice were also supplemented with tetrahydrobiopterin and pathophysiology was assessed. Results Duchenne muscular dystrophy patients had lower urinary dihydrobiopterin + tetrahydrobiopterin/specific gravity 1.020 compared to unaffected age‐matched males and Becker muscular dystrophy patients. Mdx mice had low urinary and skeletal muscle dihydrobiopterin + tetrahydrobiopterin compared to wild‐type mice. Overexpression of dystrophins that localize neuronal nitric oxide synthase restored dihydrobiopterin + tetrahydrobiopterin in mdx mice to wild‐type levels while utrophin overexpression did not. Mdx mice and Duchenne muscular dystrophy patients did not increase tetrahydrobiopterin during exercise and in mdx mice tetrahydrobiopterin deficiency was likely because of lower levels of sepiapterin reductase in skeletal muscle. Tetrahydrobiopterin supplementation improved skeletal muscle strength, resistance to fatiguing and injurious contractions in vivo, increased utrophin and capillary density of skeletal muscle and lowered cardiac muscle fibrosis and left ventricular wall thickness in mdx mice. Conclusion These data demonstrate that impaired tetrahydrobiopterin synthesis is associated with dystrophin loss and treatment with tetrahydrobiopterin improves striated muscle histopathology and skeletal muscle function in mdx mice.
    Type of Medium: Online Resource
    ISSN: 1748-1708 , 1748-1716
    URL: Issue
    URL: Article
    DOI: 10.1111/apha.2021.231.issue-4
    DOI: 10.1111/apha.13627
    Language: English
    Publisher: Wiley
    Publication Date: 2021
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  • 5
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    Impact of estrogen deficiency on diaphragm and leg muscle contractile function in female mdx mice
    Public Library of Science (PLoS) ; 2021
    In:  PLOS ONE Vol. 16, No. 3 ( 2021-3-31), p. e0249472-
    Details
    In: PLOS ONE, Public Library of Science (PLoS), Vol. 16, No. 3 ( 2021-3-31), p. e0249472-
    Abstract: Female carriers of Duchenne muscular dystrophy (DMD) presenting with DMD symptomology similar to males with DMD, such as skeletal muscle weakness and cardiomyopathy, are termed manifesting carriers. There is phenotypic variability among manifesting carriers including the age of onset, which can range from the first to fourth decade of life. In females, estrogen levels typically begin to decline during the fourth decade of life and estrogen deficiency contributes to loss of muscle strength and recovery of strength following injury. Thus, we questioned whether the decline of estrogen impacts the development of DMD symptoms in females. To address this question, we studied 6–8 month-old homozygous mdx female mice randomly assigned to a sham or ovariectomy (OVX) surgical group. In vivo whole-body plethysmography assessed ventilatory function and diaphragm muscle strength was measured in vitro before and after fatigue. Anterior crural muscles were analyzed in vivo for contractile function, fatigue, and in response to eccentric contraction (ECC)-induced injury. For the latter, 50 maximal ECCs were performed by the anterior crural muscles to induce injury. Body mass, uterine mass, hypoxia-hypercapnia ventilatory response, and fatigue index were analyzed by a pooled unpaired t-test. A two-way ANOVA was used to analyze ventilatory measurements. Fatigue and ECC-injury recovery experiments were analyzed by a two-way repeated-measures ANOVA. Results show no differences between sham and OVX mdx mice in ventilatory function, strength, or recovery of strength after fatigue in the diaphragm muscle or anterior crural muscles (p ≥ 0.078). However, OVX mice had significantly greater eccentric torque loss and blunted recovery of strength after ECC-induced injury compared to sham mice (p ≤ 0.019). Although the results show that loss of estrogen has minimal impact on skeletal muscle contractile function in female mdx mice, a key finding suggests that estrogen is important in muscle recovery in female mdx mice after injury.
    Type of Medium: Online Resource
    ISSN: 1932-6203
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.1371/journal.pone.0249472
    DOI: 10.1371/journal.pone.0249472.g001
    DOI: 10.1371/journal.pone.0249472.g002
    DOI: 10.1371/journal.pone.0249472.g003
    DOI: 10.1371/journal.pone.0249472.g004
    DOI: 10.1371/journal.pone.0249472.g005
    DOI: 10.1371/journal.pone.0249472.t001
    Language: English
    Publisher: Public Library of Science (PLoS)
    Publication Date: 2021
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  • 6
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    Preservation of satellite cell number and regenerative potential with age reveals locomotory muscle bias
    Springer Science and Business Media LLC ; 2021
    In:  Skeletal Muscle Vol. 11, No. 1 ( 2021-12)
    Details
    In: Skeletal Muscle, Springer Science and Business Media LLC, Vol. 11, No. 1 ( 2021-12)
    Abstract: Although muscle regenerative capacity declines with age, the extent to which this is due to satellite cell-intrinsic changes vs. environmental changes has been controversial. The majority of aging studies have investigated hindlimb locomotory muscles, principally the tibialis anterior, in caged sedentary mice, where those muscles are abnormally under-exercised. Methods We analyze satellite cell numbers in 8 muscle groups representing locomotory and non-locomotory muscles in young and 2-year-old mice and perform transplantation assays of low numbers of hind limb satellite cells from young and old mice. Results We find that satellite cell density does not decline significantly by 2 years of age in most muscles, and one muscle, the masseter, shows a modest but statistically significant increase in satellite cell density with age. The tibialis anterior and extensor digitorum longus were clear exceptions, showing significant declines. We quantify self-renewal using a transplantation assay. Dose dilution revealed significant non-linearity in self-renewal above a very low threshold, suggestive of competition between satellite cells for space within the pool. Assaying within the linear range, i.e., transplanting fewer than 1000 cells, revealed no evidence of decline in cell-autonomous self-renewal or regenerative potential of 2-year-old murine satellite cells. Conclusion These data demonstrate the value of comparative muscle analysis as opposed to overreliance on locomotory muscles, which are not used physiologically in aging sedentary mice, and suggest that self-renewal impairment with age is precipitously acquired at the geriatric stage, rather than being gradual over time, as previously thought.
    Type of Medium: Online Resource
    ISSN: 2044-5040
    URL: Article
    DOI: 10.1186/s13395-021-00277-2
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2021
    detail.hit.zdb_id: 2595637-1
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  • 7
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    Isometric resistance training increases strength and alters histopathology of dystrophin-deficient mouse skeletal muscle
    American Physiological Society ; 2019
    In:  Journal of Applied Physiology Vol. 126, No. 2 ( 2019-02-01), p. 363-375
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 126, No. 2 ( 2019-02-01), p. 363-375
    Abstract: Mutation to the dystrophin gene causes skeletal muscle weakness in patients with Duchenne muscular dystrophy (DMD) or Becker muscular dystrophy (BMD). Deliberation continues regarding implications of prescribing exercise for these patients. The purpose of this study was to determine whether isometric resistance exercise (~10 tetanic contractions/session) improves skeletal muscle strength and histopathology in the mdx mouse model of DMD. Three isometric training sessions increased in vivo isometric torque (22%) and contractility rates (54%) of anterior crural muscles of mdx mice. Mice expressing a BMD-causing missense mutated dystrophin on the mdx background showed comparable increases in torque (22%), while wild-type mice showed less change (11%). Increases in muscle function occurred within 1 h and peaked 3 days posttraining; however, the adaptation was lost after 7 days unless retrained. Six isometric training sessions over 4 wk caused increased isometric torque (28%) and contractility rates (22–28%), reduced fibrosis, as well as greater uniformity of fiber cross-sectional areas, fewer embryonic myosin heavy-chain-positive fibers, and more satellite cells in tibialis anterior muscle compared with the contralateral untrained muscle. Ex vivo functional analysis of isolated extensor digitorum longus (EDL) muscle from the trained hindlimb revealed greater absolute isometric force, lower passive stiffness, and a lower susceptibility to eccentric contraction-induced force loss compared with untrained EDL muscle. Overall, these data support the concept that exercise training in the form of isometric tetanic contractions can improve contractile function of dystrophin-deficient muscle, indicating a potential role for enhancing muscle strength in patients with DMD and BMD. NEW & NOTEWORTHY We focused on adaptive responses of dystrophin-deficient mouse skeletal muscle to isometric contraction training and report that in the absence of dystrophin (or in the presence of a mutated dystrophin), strength and muscle histopathology are improved. Results suggest that the strength gains are associated with fiber hypertrophy, reduced fibrosis, increased number of satellite cells, and blunted eccentric contraction-induced force loss in vitro. Importantly, there was no indication that the isometric exercise training was deleterious to dystrophin-deficient muscle.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00948.2018
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2019
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  • 8
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    Variable cytoplasmic actin expression impacts the sensitivity of different dystrophin‐deficient mdx skeletal muscles to eccentric contraction
    Wiley ; 2019
    In:  The FEBS Journal Vol. 286, No. 13 ( 2019-07), p. 2562-2576
    Details
    In: The FEBS Journal, Wiley, Vol. 286, No. 13 ( 2019-07), p. 2562-2576
    Abstract: Eccentric contractions ( ECCs ) induce force loss in several skeletal muscles of dystrophin‐deficient mice ( mdx ), with the exception of the soleus (Sol). The eccentric force : isometric force ( ECC  :  ISO ), expression level of utrophin, fiber type distribution, and sarcoendoplasmic reticulum calcium ATPase expression are factors that differ between muscles and may contribute to the sensitivity of mdx skeletal muscle to ECC . Here, we confirm that the Sol of mdx mice loses only 13% force compared to 87% in the extensor digitorum longus ( EDL ) following 10 ECC of isolated muscles. The Sol has a greater proportion of fibers expressing Type I myosin heavy chain (MHC) and expresses 2.3‐fold more utrophin compared to the EDL . To examine the effect of ECC : ISO , we show that the mdx Sol is insensitive to ECC at ECC : ISO up to 230 ± 15%. We show that the peroneus longus (PL) muscle presents with similar ECC : ISO compared to the EDL , intermediate force loss (68%) following 10 ECC , and intermediate fiber type distribution and utrophin expression relative to EDL and Sol. The combined absence of utrophin and dystrophin in mdx /utrophin −/− mice rendered the Sol only partially susceptible to ECC and exacerbated force loss in the EDL and PL . Most interestingly, the expression levels of cytoplasmic β‐ and γ‐actins correlate inversely with a given muscle's sensitivity to ECC ; EDL   〈   PL   〈  Sol. Our data indicate that fiber type, utrophin, and cytoplasmic actin expression all contribute to the differential sensitivities of mdx EDL , PL , and Sol muscles to ECC .
    Type of Medium: Online Resource
    ISSN: 1742-464X , 1742-4658
    URL: Issue
    URL: Article
    DOI: 10.1111/febs.2019.286.issue-13
    DOI: 10.1111/febs.14831
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 2173655-8
    detail.hit.zdb_id: 2172518-4
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  • 9
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    Effects of Dexamethasone Dose and Timing on Tissue-Engineered Skeletal Muscle Units
    S. Karger AG ; 2018
    In:  Cells Tissues Organs Vol. 205, No. 4 ( 2018), p. 197-207
    Details
    In: Cells Tissues Organs, S. Karger AG, Vol. 205, No. 4 ( 2018), p. 197-207
    Abstract: Our lab showed that administration of dexamethasone (DEX) stimulated myogenesis and resulted in advanced structure in our engineered skeletal muscle units (SMU). While administration of 25 nM DEX resulted in the most advanced structure, 10 nM dosing resulted in the greatest force production. We hypothesized that administration of 25 nM DEX during the entire fabrication process was toxic to the cells and that administration of DEX at precise time points during myogenesis would result in SMU with a more advanced structure and function. Thus, we fabricated SMU with 25 nM DEX administered at early proliferation (days 0–4), late proliferation (days 3–5), and early differentiation (days 5–7) stages of myogenesis and compared them to SMU treated with 10 nM DEX (days 0–16). Cell proliferation was measured with a BrdU assay (day 4) and myogenesis was examined by immunostaining for MyoD (day 4), myogenin (day 7), and α-actinin (day 11). Following SMU formation, isometric tetanic force production was measured. An analysis of cell proliferation indicated that 25 nM DEX administered at early proliferation (days 0–4) provided 21.5% greater myogenic proliferation than 10 nM DEX (days 0–4). In addition, 25 nM DEX administered at early differentiation (days 5–7) showed the highest density of myogenin-positive cells, demonstrating the greatest improvement in differentiation of myoblasts. However, the most advanced sarcomeric structure and the highest force production were exhibited with sustained administration of 10 nM DEX (days 0–16). In conclusion, alteration of the timing of 25 nM DEX administration did not enhance the structure or function of our SMU. SMU were optimally fabricated with sustained administration of 10 nM DEX.
    Type of Medium: Online Resource
    ISSN: 1422-6405 , 1422-6421
    URL: Article
    DOI: 10.1159/000490884
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2018
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    detail.hit.zdb_id: 1468141-9
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