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  • 1
    Online Resource
    Online Resource
    Massage as a mechanotherapy promotes skeletal muscle protein and ribosomal turnover but does not mitigate muscle atrophy during disuse in adult rats
    Wiley ; 2020
    In:  Acta Physiologica Vol. 229, No. 3 ( 2020-07)
    Details
    In: Acta Physiologica, Wiley, Vol. 229, No. 3 ( 2020-07)
    Abstract: Interventions that decrease atrophy during disuse are desperately needed to maintain muscle mass. We recently found that massage as a mechanotherapy can improve muscle regrowth following disuse atrophy. Therefore, we aimed to determine if massage has similar anabolic effects when applied during normal weight bearing conditions (WB) or during atrophy induced by hindlimb suspension (HS) in adult rats. Methods Adult (10 months) male Fischer344‐Brown Norway rats underwent either hindlimb suspension (HS, n = 8) or normal WB (WB, n = 8) for 7 days. Massage was applied using cyclic compressive loading (CCL) in WB (WBM, n = 9) or HS rats (HSM, n = 9) and included four 30‐minute bouts of CCL applied to gastrocnemius muscle every other day. Results Massage had no effect on any anabolic parameter measured under WB conditions (WBM). In contrast, massage during HS (HSM) stimulated protein turnover, but did not mitigate muscle atrophy. Atrophy from HS was caused by both lowered protein synthesis and higher degradation. HS and HSM had lowered total RNA compared with WB and this was the result of significantly higher ribosome degradation in HS that was attenuated in HSM, without differences in ribosomal biogenesis. Also, massage increased protein turnover in the non‐massaged contralateral limb during HS. Finally, we determined that total RNA degradation primarily dictates loss of muscle ribosomal content during disuse atrophy. Conclusion We conclude that massage is an effective mechanotherapy to impact protein turnover during muscle disuse in both the massaged and non‐massaged contralateral muscle, but it does not attenuate the loss of muscle mass.
    Type of Medium: Online Resource
    ISSN: 1748-1708 , 1748-1716
    URL: Issue
    URL: Article
    DOI: 10.1111/apha.v229.3
    DOI: 10.1111/apha.13460
    Language: English
    Publisher: Wiley
    Publication Date: 2020
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  • 2
    Online Resource
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    Muscle from aged rats is resistant to mechanotherapy during atrophy and reloading
    Springer Science and Business Media LLC ; 2021
    In:  GeroScience Vol. 43, No. 1 ( 2021-02), p. 65-83
    Details
    In: GeroScience, Springer Science and Business Media LLC, Vol. 43, No. 1 ( 2021-02), p. 65-83
    Type of Medium: Online Resource
    ISSN: 2509-2715 , 2509-2723
    URL: Article
    DOI: 10.1007/s11357-020-00215-y
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2021
    detail.hit.zdb_id: 2886418-9
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  • 3
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    Extracellular vesicle distribution and localization in skeletal muscle at rest and following disuse atrophy
    Springer Science and Business Media LLC ; 2023
    In:  Skeletal Muscle Vol. 13, No. 1 ( 2023-03-10)
    Details
    In: Skeletal Muscle, Springer Science and Business Media LLC, Vol. 13, No. 1 ( 2023-03-10)
    Abstract: Skeletal muscle (SkM) is a large, secretory organ that produces and releases myokines that can have autocrine, paracrine, and endocrine effects. Whether extracellular vesicles (EVs) also play a role in the SkM adaptive response and ability to communicate with other tissues is not well understood. The purpose of this study was to investigate EV biogenesis factors, marker expression, and localization across cell types in the skeletal muscle. We also aimed to investigate whether EV concentrations are altered by disuse atrophy. Methods To identify the potential markers of SkM-derived EVs, EVs were isolated from rat serum using density gradient ultracentrifugation, followed by fluorescence correlation spectroscopy measurements or qPCR. Single-cell RNA sequencing (scRNA-seq) data from rat SkM were analyzed to assess the EV biogenesis factor expression, and cellular localization of tetraspanins was investigated by immunohistochemistry. Finally, to assess the effects of mechanical unloading on EV expression in vivo, EV concentrations were measured in the serum by nanoparticle tracking analysis in both a rat and human model of disuse. Results In this study, we show that the widely used markers of SkM-derived EVs, α-sarcoglycan and miR-1, are undetectable in serum EVs. We also found that EV biogenesis factors, including the tetraspanins CD63, CD9, and CD81, are expressed by a variety of cell types in SkM. SkM sections showed very low detection of CD63, CD9, and CD81 in myofibers and instead accumulation within the interstitial space. Furthermore, although there were no differences in serum EV concentrations following hindlimb suspension in rats, serum EV concentrations were elevated in human subjects after bed rest. Conclusions Our findings provide insight into the distribution and localization of EVs in SkM and demonstrate the importance of methodological guidelines in SkM EV research.
    Type of Medium: Online Resource
    ISSN: 2044-5040
    URL: Article
    DOI: 10.1186/s13395-023-00315-1
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 2595637-1
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  • 4
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    Serial Passaging Reduces Replication and Fusion Capacity of Primary Human Skeletal Muscle Satellite Cells : 2261 Board #97 June 1 9 30 AM - 11 00 AM
    Ovid Technologies (Wolters Kluwer Health) ; 2018
    In:  Medicine & Science in Sports & Exercise Vol. 50, No. 5S ( 2018-05), p. 552-
    Details
    In: Medicine & Science in Sports & Exercise, Ovid Technologies (Wolters Kluwer Health), Vol. 50, No. 5S ( 2018-05), p. 552-
    Type of Medium: Online Resource
    ISSN: 0195-9131
    URL: Article
    DOI: 10.1249/01.mss.0000536908.31955.88
    RVK:
    ZX 1000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2018
    detail.hit.zdb_id: 2031167-9
    SSG: 31
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  • 5
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    Skeletal muscle RBM3 expression is associated with extended lifespan in Ames Dwarf and calorie restricted mice
    Elsevier BV ; 2021
    In:  Experimental Gerontology Vol. 146 ( 2021-04), p. 111214-
    Details
    In: Experimental Gerontology, Elsevier BV, Vol. 146 ( 2021-04), p. 111214-
    Type of Medium: Online Resource
    ISSN: 0531-5565
    URL: Article
    DOI: 10.1016/j.exger.2020.111214
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2021
    detail.hit.zdb_id: 2005397-6
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  • 6
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    Bioengineered 3D Skeletal Muscle Model Reveals Complement 4b as a Cell‐Autonomous Mechanism of Impaired Regeneration with Aging
    Wiley ; 2023
    In:  Advanced Materials Vol. 35, No. 17 ( 2023-04)
    Details
    In: Advanced Materials, Wiley, Vol. 35, No. 17 ( 2023-04)
    Abstract: A mechanistic understanding of cell‐autonomous skeletal muscle changes after injury can lead to novel interventions to improve functional recovery in an aged population. However, major knowledge gaps persist owing to limitations of traditional biological aging models. 2D cell culture represents an artificial environment, while aging mammalian models are contaminated by influences from non‐muscle cells and other organs. Here, a 3D muscle aging system is created to overcome the limitations of these traditional platforms. It is shown that old muscle constructs (OMC) manifest a sarcopenic phenotype, as evidenced by hypotrophic myotubes, reduced contractile function, and decreased regenerative capacity compared to young muscle constructs. OMC also phenocopy the regenerative responses of aged muscle to two interventions, pharmacological and biological. Interrogation of muscle cell‐specific mechanisms that contribute to impaired regeneration over time further reveals that an aging‐induced increase of complement component 4b (C4b) delays muscle progenitor cell amplification and impairs functional recovery. However, administration of complement factor I, a C4b inactivator, improves muscle regeneration in vitro and in vivo, indicating that C4b inhibition may be a novel approach to enhance aged muscle repair. Collectively, the model herein exhibits capabilities to study cell‐autonomous changes in skeletal muscle during aging, regeneration, and intervention.
    Type of Medium: Online Resource
    ISSN: 0935-9648 , 1521-4095
    URL: Issue
    URL: Article
    DOI: 10.1002/adma.v35.17
    DOI: 10.1002/adma.202207443
    RVK:
    UA 1538
    Language: English
    Publisher: Wiley
    Publication Date: 2023
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  • 7
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    Impaired proteostatic mechanisms other than decreased protein synthesis limit old skeletal muscle recovery after disuse atrophy
    Wiley ; 2023
    In:  Journal of Cachexia, Sarcopenia and Muscle
    Details
    In: Journal of Cachexia, Sarcopenia and Muscle, Wiley
    Abstract: Skeletal muscle mass and strength diminish during periods of disuse but recover upon return to weight bearing in healthy adults but are incomplete in old muscle. Efforts to improve muscle recovery in older individuals commonly aim at increasing myofibrillar protein synthesis via mammalian target of rapamycin (mTOR) stimulation despite evidence demonstrating that old muscle has chronically elevated levels of mammalian target of rapamycin complex 1 (mTORC1) activity. We hypothesized that protein synthesis is higher in old muscle than adult muscle, which contributes to a proteostatic stress that impairs recovery. Methods We unloaded hindlimbs of adult (10‐month) and old (28‐month) F344BN rats for 14 days to induce atrophy, followed by reloading up to 60 days with deuterium oxide (D 2 O) labelling to study muscle regrowth and proteostasis. Results We found that old muscle has limited recovery of muscle mass during reloading despite having higher translational capacity and myofibrillar protein synthesis (0.029  k /day ± 0.002 vs. 0.039  k /day ± 0.002, P   〈  0.0001) than adult muscle. We showed that collagen protein synthesis was not different (0.005  k (1/day) ± 0.0005 vs. 0.004  k (1/day) ± 0.0005, P  = 0.15) in old compared to adult, but old muscle had higher collagen concentration (4.5 μg/mg ± 1.2 vs. 9.8 μg/mg ± 0.96, P   〈  0.01), implying that collagen breakdown was slower in old muscle than adult muscle. This finding was supported by old muscle having more insoluble collagen (4.0 ± 1.1 vs. 9.2 ± 0.9, P   〈 0.01) and an accumulation of advanced glycation end products (1.0 ± 0.06 vs. 1.5 ± 0.08, P   〈  0.001) than adult muscle during reloading. Limited recovery of muscle mass during reloading is in part due to higher protein degradation (0.017 1/ t  ± 0.002 vs. 0.028 1/ t  ± 0.004, P   〈  0.05) and/or compromised proteostasis as evidenced by accumulation of ubiquitinated insoluble proteins (1.02 ± 0.06 vs. 1.22 ± 0.06, P   〈  0.05). Last, we showed that synthesis of individual proteins related to protein folding/refolding, protein degradation and neural‐related biological processes was higher in old muscle during reloading than adult muscle. Conclusions Our data suggest that the failure of old muscle to recover after disuse is not due to limitations in the ability to synthesize myofibrillar proteins but because of other impaired proteostatic mechanisms (e.g., protein folding and degradation). These data provide novel information on individual proteins that accumulate in protein aggregates after disuse and certain biological processes such as protein folding and degradation that likely play a role in impaired recovery. Therefore, interventions to enhance regrowth of old muscle after disuse should be directed towards the identified impaired proteostatic mechanisms and not aimed at increasing protein synthesis.
    Type of Medium: Online Resource
    ISSN: 2190-5991 , 2190-6009
    URL: Article
    DOI: 10.1002/jcsm.13285
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2586864-0
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  • 8
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    Extracellular vesicles released from stress‐induced prematurely senescent myoblasts impair endothelial function and proliferation
    Wiley ; 2021
    In:  Experimental Physiology Vol. 106, No. 10 ( 2021-10), p. 2083-2095
    Details
    In: Experimental Physiology, Wiley, Vol. 106, No. 10 ( 2021-10), p. 2083-2095
    Abstract: What is the central question of this study? What is the impact of stress‐induced premature senescence on skeletal muscle myoblast‐derived extracellular vesicles (EVs) and myoblast–endothelial cell crosstalk? What is the main finding and its importance? Hydrogen peroxide treatment of human myoblasts induced stress‐induced premature senescence (SIPS) and increased the release of exosome‐sized EVs (30–150 nm in size) five‐fold compared to untreated controls. Treatment of SIPS myoblast‐derived EVs on endothelial cells increased senescence markers and decreased proliferation. Gene expression analysis of SIPS myoblast‐derived EVs revealed a four‐fold increase in senescence factor transforming growth factor‐β. These results highlight potential mechanisms by which senescence imparts deleterious effects on the cellular microenvironment. Abstract Cellular senescence contributes to numerous diseases through the release of pro‐inflammatory factors as part of the senescence‐associated secretory phenotype (SASP). In skeletal muscle, resident muscle progenitor cells (satellite cells) express markers of senescence with advancing age and in response to various pathologies, which contributes to reduced regenerative capacities in vitro. Satellite cells regulate their microenvironment in part through the release of extracellular vesicles (EVs), but the effect of senescence on EV signaling is unknown. Primary human myoblasts were isolated following biopsies of the vastus lateralis from young healthy subjects. Hydrogen peroxide (H 2 O 2 ) treatment was used to achieve stress‐induced premature senescence (SIPS) of myoblasts. EVs secreted by myoblasts with and without H 2 O 2 treatment were isolated, analysed and used to treat human umbilical vein endothelial cells (HUVECs) to assess senescence and angiogenic impact. H 2 O 2 treatment of primary human myoblasts in vitro increased markers of senescence (β‐galactosidase and p21 Cip1 ), decreased proliferation and increased exosome‐like EV (30–150 nm) release approximately five‐fold. In HUVECs, EV treatment from H 2 O 2 ‐treated myoblasts increased markers of senescence (β‐galactosidase and transforming growth factor β), decreased proliferation and impaired HUVEC tube formation. Analysis of H 2 O 2 ‐treated myoblast‐derived EV mRNA revealed a nearly four‐fold increase in transforming growth factor β expression. Our novel results highlight the impact of SIPS on myoblast communication and identify a VasoMyo Crosstalk by which SIPS myoblast‐derived EVs impair endothelial cell function in vitro.
    Type of Medium: Online Resource
    ISSN: 0958-0670 , 1469-445X
    URL: Issue
    URL: Article
    DOI: 10.1113/eph.v106.10
    DOI: 10.1113/EP089423
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 1493802-9
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  • 9
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    The transcript interactome of skeletal muscle RNA binding protein motif 3 ( RBM3 )
    Wiley ; 2023
    In:  Physiological Reports Vol. 11, No. 3 ( 2023-02)
    Details
    In: Physiological Reports, Wiley, Vol. 11, No. 3 ( 2023-02)
    Abstract: Post‐transcriptional regulation of gene expression represents a critical regulatory step in the production of a functional proteome. Elevated expression of post‐transcriptional regulator RNA binding motif protein 3 (RBM3), an RNA binding protein in the cold‐shock family, is positively correlated with skeletal muscle growth in adult mice. However, mechanisms through which RBM3 exerts its effects are largely unknown. The purpose of this study was to perform RNA immunoprecipitation followed by RNA sequencing (RIP‐seq) and apply a network science approach to understand biological processes (BPs) most associated with RBM3‐bound mRNAs. In addition, through nucleotide‐sequence‐scanning of enriched transcripts, we predicted the motif for skeletal muscle RBM3 binding. Gene set enrichment analysis followed by enrichment mapping of RBM3‐bound transcripts (fold change 〉 3; p.adj   〈 0.01) revealed significant enrichment of BPs associated with “Contractile apparatus,” “Translation initiation,” and “Proteosome complex.” Clusters were driven largely by enrichment of Myh1 (FC: 4.43), Eif4b (FC: 5.03), and Trim63 (FC: 5.84), respectively. Motif scanning of enriched sequences revealed a discrete 14 nucleotide‐wide motif found most prominently at the junction between the protein coding region's termination sequence and the start of the 3′ untranslated region (UTR; E ‐Value: 1.1 e −015 ). Proof of concept investigation of motif location along enriched transcripts Myh1 and Myl4 revealed 3′ UTR binding, suggesting RBM3 involvement in transcript half‐life regulation. Together, these results demonstrate the potential influence of RBM3 in reshaping the skeletal muscle proteome through post‐transcriptional regulation of mRNAs crucial to muscle adaptations.
    Type of Medium: Online Resource
    ISSN: 2051-817X , 2051-817X
    URL: Article
    DOI: 10.14814/phy2.15596
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2724325-4
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  • 10
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    RNA-binding proteins: The next step in translating skeletal muscle adaptations?
    American Physiological Society ; 2019
    In:  Journal of Applied Physiology Vol. 127, No. 2 ( 2019-08-01), p. 654-660
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 127, No. 2 ( 2019-08-01), p. 654-660
    Abstract: The decline of skeletal muscle mass during illness, injury, disuse, and aging is associated with poor health outcomes. Therefore, it is important to pursue a greater understanding of the mechanisms that dictate skeletal muscle adaptation. In this review, we propose that RNA-binding proteins (RBPs) comprise a critical regulatory node in the orchestration of adaptive responses in skeletal muscle. While RBPs have broadly pleiotropic molecular functions, our discussion is constrained at the outset by observations from hibernating animals, which suggest that RBP regulation of RNA stability and its impact on translational reprogramming is a key component of skeletal muscle response to anabolic and catabolic stimuli. We discuss the limited data available on the expression and functions of RBPs in adult skeletal muscle in response to disuse, aging, and exercise. A model is proposed in which dynamic changes in RBPs play a central role in muscle adaptive processes through their differential effects on mRNA stability. While limited, the currently available data suggest that understanding how adaptive (and maladaptive) changes in the expression of RBPs regulate mRNA stability in skeletal muscle could be an informative and productive research area for finding new strategies to limit atrophy and promote hypertrophy.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00076.2019
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2019
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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