Journal of Muscle Research and Cell Motility最新文献

{"title":"Effect of eccentric and concentric contraction mode on myogenic regulatory factors expression in human vastus lateralis muscle.","authors":"Mostafa Sabouri,&nbsp;Pejman Taghibeikzadehbadr,&nbsp;Fatemeh Shabkhiz,&nbsp;Zahra Izanloo,&nbsp;Farahnaz Amir Shaghaghi","doi":"10.1007/s10974-021-09613-x","DOIUrl":"https://doi.org/10.1007/s10974-021-09613-x","url":null,"abstract":"<p><p>Skeletal muscle contractions are caused to release myokines by muscle fiber. This study investigated the myogenic regulatory factors, as MHC I, IIA, IIX, Myo-D, MRF4, Murf, Atrogin-1, Decorin, Myonection, and IL-15 mRNA expression in the response of eccentric vs concentric contraction. Eighteen healthy men were randomly divided into two eccentric and concentric groups, each of 9 persons. Isokinetic contraction protocols included maximal single-leg eccentric or concentric knee extension tasks at 60°/s with the dominant leg. Contractions consisted of a maximum of 12 sets of 10 reps, and the rest time between each set was 30 s. The baseline biopsy was performed 4 weeks before the study, and post-test biopsies were taken immediately after exercise protocols from the vastus lateralis muscle. The gene expression levels were evaluated using Real-Time PCR methods. The eccentric group showed a significantly lower RPE score than the concentric group (P ≤ 0.05). A significant difference in MyoD, MRF4, Myonection, and Decorin mRNA, were observed following eccentric or concentric contractions (P ≤ 0.05). The MHC I, MHC IIA, IL-15 mRNA has been changed significantly compared to the pre-exercise in the concentric group (P ≤ 0.05). While only MHC IIX and Atrogin-1 mRNA changed significantly in the eccentric group (P ≤ 0.05). Additionally, the results showed a significant difference in MyoD, MRF4, IL-15, and Decorin at the follow-up values between eccentric or concentric groups (P ≤ 0.05). Our findings highlight the growing importance of elucidating the different responses of muscle growth factors associated with a myogenic activity such as MHC IIA, Decorin, IL-15, Myonectin, Decorin, MuRF1, and MHC IIX mRNA in following various types of exercise.</p>","PeriodicalId":16422,"journal":{"name":"Journal of Muscle Research and Cell Motility","volume":" ","pages":"9-20"},"PeriodicalIF":2.7,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39674226","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of muscle-specific and metabolism regulating microRNAs in a chronic swimming rat model.","authors":"Zsuzsanna Gaál,&nbsp;János Fodor,&nbsp;Attila Oláh,&nbsp;Tamás Radovits,&nbsp;Béla Merkely,&nbsp;János Magyar,&nbsp;László Csernoch","doi":"10.1007/s10974-021-09612-y","DOIUrl":"https://doi.org/10.1007/s10974-021-09612-y","url":null,"abstract":"<p><p>Making benefit from the epigenetic effects of environmental factors such as physical activity may result in a considerable improvement in the prevention of chronic civilization diseases. In our chronic swimming rat model, the expression levels of such microRNAs were characterized, that are involved in skeletal muscle differentiation, hypertrophy and fine-tuning of metabolism, which processes are influenced by chronic endurance training, contributing to the metabolic adaptation of skeletal muscle during physical activity. After chronic swimming, the level of miR-128a increased significantly in EDL muscles, which may influence metabolic adaptation and stress response as well. In SOL, the expression level of miR-15b and miR-451 decreased significantly after chronic swimming, which changes are opposite to their previously described increment in insulin resistant skeletal muscle. MiR-451 also targets PGC-1α mRNA, whiches expression level significantly increased in SOL muscles, resulting in enhanced biogenesis and oxidative capacity of mitochondria. In summary, the microRNA expression changes that were observed during our experiments suggest that chronic swim training contributes to a beneficial metabolic profile of skeletal muscle.</p>","PeriodicalId":16422,"journal":{"name":"Journal of Muscle Research and Cell Motility","volume":" ","pages":"21-33"},"PeriodicalIF":2.7,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8897377/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39715699","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Treadmill running prevents atrophy differently in fast- versus slow-twitch muscles in a rat model of rheumatoid arthritis.","authors":"Yoichiro Kamada,&nbsp;Shogo Toyama,&nbsp;Yuji Arai,&nbsp;Hiroaki Inoue,&nbsp;Shuji Nakagawa,&nbsp;Yuta Fujii,&nbsp;Kenta Kaihara,&nbsp;Tsunao Kishida,&nbsp;Osam Mazda,&nbsp;Kenji Takahashi","doi":"10.1007/s10974-021-09610-0","DOIUrl":"https://doi.org/10.1007/s10974-021-09610-0","url":null,"abstract":"<p><p>To investigate the effects of treadmill running on two different types of skeletal muscle, we established a rat model of collagen-induced arthritis (CIA). The skeletal muscles studied were the extensor digitorum longus (EDL), which is rich in fast-twitch muscle fibers, and the soleus, which is rich in slow-twitch muscle fibers. The histological and transcriptional changes in these muscles at 14 and 44 days after immunosensitization were compared between rats that were forced to exercise (CIA ex group) and free-reared CIA rats (CIA no group). Change in protein expression was examined on day 14 after a single bout of treadmill running. Treadmill running had different effects on the relative muscle weight and total and fiber cross-sectional areas in each muscle type. In the soleus, it prevented muscle atrophy. Transcriptional analysis revealed increased eukaryotic translation initiation factor 4E (Eif4e) expression on day 14 and increased Atrogin-1 and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) expression on day 44 in the soleus in the CIA ex group, suggesting an interaction between muscle type and exercise. A single bout of treadmill running increased the level of Eif4e and p70S6K and decreased that of Atrogin-1 in the soleus on day 14. Treadmill running prevented muscle atrophy in the soleus in a rat model of rheumatoid arthritis via activation of mitochondrial function, as evidenced by increased PGC-1α expression.</p>","PeriodicalId":16422,"journal":{"name":"Journal of Muscle Research and Cell Motility","volume":"42 3-4","pages":"429-441"},"PeriodicalIF":2.7,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39549077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Organisational alteration of cardiac myofilament proteins by hyperglycaemia in mouse embryonic stem cell-derived cardiomyocytes.","authors":"Hamida Aboalgasm,&nbsp;Robea Ballo,&nbsp;Asfree Gwanyanya","doi":"10.1007/s10974-021-09607-9","DOIUrl":"https://doi.org/10.1007/s10974-021-09607-9","url":null,"abstract":"<p><p>The exposure of the developing foetal heart to hyperglycaemia in mothers with diabetes mellitus is a major risk factor for foetal cardiac complications that lead to heart failure. We studied the effects of hyperglycaemia on the layout of cardiac myofilament proteins in stem cell-derived cardiomyocytes and their possible underlying mechanisms. Mouse embryonic stem cells (mESCs) were differentiated into cardiac-like cells and cultured in media containing baseline- or high glucose concentrations. Cellular biomarkers were detected using Western blot analysis, immunocytochemistry, 5-ethynyl-2'-deoxyuridine (EdU) cell proliferation assay, and terminal deoxynucleotidyl transferase dUTP nick-end labelling (TUNEL) assay. High glucose decreased the proportion of cardiac troponin T and α-actinin 2 positive mESCs as well as disrupted the α-actinin 2 striated pattern and the distribution of the cardiac myosin heavy chain α- and β isoforms. However, there was no alteration of the cellular EdU uptake nor the expression of the receptor of advanced glycation end-product (RAGE). High glucose also increased the presence of the oxidative stress marker nitrotyrosine as well as the number of TUNEL-stained nuclei in cardiac-like cells. Treatment with the antioxidant N-acetyl cysteine decreased the number of TUNEL-stained cells in high glucose and improved the α-actinin 2 striated pattern. Hyperglycaemia negatively impacted the expression and cellular organisation of cardiac myofilament proteins in mESC-derived cardiomyocytes through oxidative stress. The results add further insights into the pathophysiological mechanisms of cardiac contractile dysfunction in diabetic cardiac developmental disease.</p>","PeriodicalId":16422,"journal":{"name":"Journal of Muscle Research and Cell Motility","volume":"42 3-4","pages":"419-428"},"PeriodicalIF":2.7,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s10974-021-09607-9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39307478","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficacy of passive repetitive stretching of skeletal muscle on myofiber hypertrophy and genetic suppression on MAFbx, MuRF1, and myostatin.","authors":"Yumin Wang,&nbsp;Satoshi Ikeda,&nbsp;Katsunori Ikoma","doi":"10.1007/s10974-021-09609-7","DOIUrl":"https://doi.org/10.1007/s10974-021-09609-7","url":null,"abstract":"<p><p>Skeletal muscles undergo adaptations in response to mechanical stimuli such as stretching. However, there is limited evidence regarding the hypertrophic effects of passive repetitive stretching in vivo. We examined the effect of passive repetitive stretching on skeletal muscle myofiber morphology, satellite cell content, and messenger RNA expression of myogenic regulatory factors and signaling molecules involved in muscle protein synthesis and degradation. The gastrocnemius muscles of mice were stretched 15 times/min by manual ankle dorsiflexion for 15 min, 5 days a week for 2 weeks. We found that passive repetitive stretching significantly increased myofiber cross-sectional area. In stretched gastrocnemius muscles, the messenger RNA expression of p70S6K and myogenin was upregulated, whereas MuRF1, MAFbx, myostatin, and 4E-BP1 were downregulated. The phosphorylation level of p70S6K was significantly increased in stretched muscles. The number of Pax7+ cells was unaffected. Passive repetitive stretching induces muscle hypertrophy by regulating signaling pathways involved in muscle protein turnover. These findings are applicable to clinical muscle strengthening and for the maintenance of skeletal muscle mass and function in patients who are unconscious or paralyzed.</p>","PeriodicalId":16422,"journal":{"name":"Journal of Muscle Research and Cell Motility","volume":"42 3-4","pages":"443-451"},"PeriodicalIF":2.7,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39529744","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Calsequestrin, a key protein in striated muscle health and disease.","authors":"Daniela Rossi,&nbsp;Alessandra Gamberucci,&nbsp;Enrico Pierantozzi,&nbsp;Caterina Amato,&nbsp;Loredana Migliore,&nbsp;Vincenzo Sorrentino","doi":"10.1007/s10974-020-09583-6","DOIUrl":"https://doi.org/10.1007/s10974-020-09583-6","url":null,"abstract":"<p><p>Calsequestrin (CASQ) is the most abundant Ca²⁺ binding protein localized in the sarcoplasmic reticulum (SR) of skeletal and cardiac muscle. The genome of vertebrates contains two genes, CASQ1 and CASQ2. CASQ1 and CASQ2 have a high level of homology, but show specific patterns of expression. Fast-twitch skeletal muscle fibers express only CASQ1, both CASQ1 and CASQ2 are present in slow-twitch skeletal muscle fibers, while CASQ2 is the only protein present in cardiomyocytes. Depending on the intraluminal SR Ca²⁺ levels, CASQ monomers assemble to form large polymers, which increase their Ca²⁺ binding ability. CASQ interacts with triadin and junctin, two additional SR proteins which contribute to localize CASQ to the junctional region of the SR (j-SR) and also modulate CASQ ability to polymerize into large macromolecular complexes. In addition to its ability to bind Ca²⁺ in the SR, CASQ appears also to be able to contribute to regulation of Ca²⁺ homeostasis in muscle cells. Both CASQ1 and CASQ2 are able to either activate and inhibit the ryanodine receptors (RyRs) calcium release channels, likely through their interactions with junctin and triadin. Additional evidence indicates that CASQ1 contributes to regulate the mechanism of store operated calcium entry in skeletal muscle via a direct interaction with the Stromal Interaction Molecule 1 (STIM1). Mutations in CASQ2 and CASQ1 have been identified, respectively, in patients with catecholamine-induced polymorphic ventricular tachycardia and in patients with some forms of myopathy. This review will highlight recent developments in understanding CASQ1 and CASQ2 in health and diseases.</p>","PeriodicalId":16422,"journal":{"name":"Journal of Muscle Research and Cell Motility","volume":"42 2","pages":"267-279"},"PeriodicalIF":2.7,"publicationDate":"2021-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s10974-020-09583-6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38001243","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Calcium entry units (CEUs): perspectives in skeletal muscle function and disease.","authors":"Feliciano Protasi,&nbsp;Laura Pietrangelo,&nbsp;Simona Boncompagni","doi":"10.1007/s10974-020-09586-3","DOIUrl":"https://doi.org/10.1007/s10974-020-09586-3","url":null,"abstract":"<p><p>In the last decades the term Store-operated Ca²⁺ entry (SOCE) has been used in the scientific literature to describe an ubiquitous cellular mechanism that allows recovery of calcium (Ca²⁺) from the extracellular space. SOCE is triggered by a reduction of Ca²⁺ content (i.e. depletion) in intracellular stores, i.e. endoplasmic or sarcoplasmic reticulum (ER and SR). In skeletal muscle the mechanism is primarily mediated by a physical interaction between stromal interaction molecule-1 (STIM1), a Ca²⁺ sensor located in the SR membrane, and ORAI1, a Ca²⁺-permeable channel of external membranes, located in transverse tubules (TTs), the invaginations of the plasma membrane (PM) deputed to propagation of action potentials. It is generally accepted that in skeletal muscle SOCE is important to limit muscle fatigue during repetitive stimulation. We recently discovered that exercise promotes the assembly of new intracellular junctions that contains colocalized STIM1 and ORAI1, and that the presence of these new junctions increases Ca²⁺ entry via ORAI1, while improving fatigue resistance during repetitive stimulation. Based on these findings we named these new junctions Ca²⁺ Entry Units (CEUs). CEUs are dynamic organelles that assemble during muscle activity and disassemble during recovery thanks to the plasticity of the SR (containing STIM1) and the elongation/retraction of TTs (bearing ORAI1). Interestingly, similar structures described as SR stacks were previously reported in different mouse models carrying mutations in proteins involved in Ca²⁺ handling (calsequestrin-null mice; triadin and junctin null mice, etc.) or associated to microtubules (MAP6 knockout mice). Mutations in Stim1 and Orai1 (and calsequestrin-1) genes have been associated to tubular aggregate myopathy (TAM), a muscular disease characterized by: (a) muscle pain, cramping, or weakness that begins in childhood and worsens over time, and (b) the presence of large accumulations of ordered SR tubes (tubular aggregates, TAs) that do not contain myofibrils, mitochondria, nor TTs. Interestingly, TAs are also present in fast twitch muscle fibers of ageing mice. Several important issues remain un-answered: (a) the molecular mechanisms and signals that trigger the remodeling of membranes and the functional activation of SOCE during exercise are unclear; and (b) how dysfunctional SOCE and/or mutations in Stim1, Orai1 and calsequestrin (Casq1) genes lead to the formation of tubular aggregates (TAs) in aging and disease deserve investigation.</p>","PeriodicalId":16422,"journal":{"name":"Journal of Muscle Research and Cell Motility","volume":"42 2","pages":"233-249"},"PeriodicalIF":2.7,"publicationDate":"2021-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s10974-020-09586-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38276130","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Voluntary exercise does not improve muscular properties or functional capacity during C26-induced cancer cachexia in mice.","authors":"Charlotte Hiroux,&nbsp;Sebastiaan Dalle,&nbsp;Katrien Koppo,&nbsp;Peter Hespel","doi":"10.1007/s10974-021-09599-6","DOIUrl":"https://doi.org/10.1007/s10974-021-09599-6","url":null,"abstract":"<p><p>Exercise training is considered as a potential intervention to counteract muscle degeneration in cancer cachexia. However, evidence to support such intervention is equivocal. Therefore, we investigated the effect of exercise training, i.e. voluntary wheel running, on muscle wasting, functional capacity, fiber type composition and vascularization during experimental cancer cachexia in mice. Balb/c mice were injected with PBS (CON) or C26 colon carcinoma cells to induce cancer cachexia (C26). Mice had free access to a running wheel in their home cage (CON_EX and C26_EX, n = 8-9) or were sedentary (CON_S and C26_S, n = 8-9). Mice were sacrificed 18 days upon tumor cell injection. Immunohistochemical analyes were performed on m. gastrocnemius and quadriceps, and ex vivo contractile properties were assessed in m. soleus and extensor digitorum longus (EDL). Compared with CON, C26 mice exhibited body weight loss (~ 20 %), muscle atrophy (~ 25 %), reduced grip strength (~ 25 %), and lower twitch and tetanic force (~ 20 %) production in EDL but not in m. soleus. Furthermore, muscle of C26 mice were characterizd by a slow-to-fast fiber type shift (type IIx fibers: +57 %) and increased capillary density (~ 30 %). In C26 mice, wheel running affect neither body weight loss, nor muscle atrophy or functional capacity, nor inhibited tumor growth. However, wheel running induced a type IIb to type IIa fiber shift in m. quadriceps from both CON and C26, but not in m. gastrocnemius. Wheel running does not exacerbate muscular degeneration in cachexic mice, but, when voluntary, is insufficient to improve the muscle phenotype.</p>","PeriodicalId":16422,"journal":{"name":"Journal of Muscle Research and Cell Motility","volume":"42 2","pages":"169-181"},"PeriodicalIF":2.7,"publicationDate":"2021-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s10974-021-09599-6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25385380","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Changes in myocardial myosin heavy chain isoform composition with exercise and post-exercise cold-water immersion.","authors":"Ramzi A Al-Horani,&nbsp;Mukhallad A Mohammad,&nbsp;Saja Haifawi,&nbsp;Mohammed Ihsan","doi":"10.1007/s10974-021-09603-z","DOIUrl":"https://doi.org/10.1007/s10974-021-09603-z","url":null,"abstract":"<p><p>This study investigated the changes in myocardial myosin heavy chain (MHC) isoforms, MHC-α and MHC-β composition in young healthy rodents following endurance training, with and without post-exercise cold-water immersion (CWI). Male rats were either trained on a treadmill for 10 weeks with (CWI) or without (Ex) regular CWI after each running session, or left sedentary (CON). Left ventricular mRNA of MHC-α, MHC-β, thyroid receptor α1 (TR-α1) and β (TR-β) were analyzed using rt-PCR and semiquantitative PCR analysis. MHC isoform protein composition was determined using SDS-PAGE electrophoresis. MHC-α isoform protein was predominant in all groups. The relative expression of MHC-β (%MHC-β) protein was not different between groups (CWI 34.7 ± 6.9%; Ex 32 ± 5.3%; CON 35.5 ± 10%; P = 0.7). MHC-β mRNA was reduced in Ex (0.7 ± 0.3-fold) compared to CWI (1.3 ± 0.2-fold; P < 0.001) and CON (1.01 ± 0.2-fold; P = 0.03). TRα1 mRNA was lower in CWI (0.4 ± 0.05-fold) than Ex (1.02 ± 0.3-fold) and CON (1.01 ± 0.2-fold) (P < 0.001 for both). CWI exhibited greater %MHC-β mRNA (56.8 ± 4.1%) than Ex (44.4 ± 7.7%; P = 0.001) and CON (48.5 ± 7.8%; P = 0.03). Neither exercise nor post-exercise CWI demonstrated a distinct effect on myocardial MHC protein isoform composition. However, CWI increased the relative expression of MHC-β mRNA compared with Ex and CON. Although this implicates a potential negative long-term impact of post-exercise CWI, future studies should include measures of cardiac function to better understand the effect of such isoform mRNA shifts following regular use of CWI.</p>","PeriodicalId":16422,"journal":{"name":"Journal of Muscle Research and Cell Motility","volume":"42 2","pages":"183-191"},"PeriodicalIF":2.7,"publicationDate":"2021-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s10974-021-09603-z","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25567481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanical loading of tissue engineered skeletal muscle prevents dexamethasone induced myotube atrophy.","authors":"Kathryn W Aguilar-Agon, Andrew J Capel, Jacob W Fleming, Darren J Player, Neil R W Martin, Mark P Lewis","doi":"10.1007/s10974-020-09589-0","DOIUrl":"10.1007/s10974-020-09589-0","url":null,"abstract":"<p><p>Skeletal muscle atrophy as a consequence of acute and chronic illness, immobilisation, muscular dystrophies and aging, leads to severe muscle weakness, inactivity and increased mortality. Mechanical loading is thought to be the primary driver for skeletal muscle hypertrophy, however the extent to which mechanical loading can offset muscle catabolism has not been thoroughly explored. In vitro 3D-models of skeletal muscle provide a controllable, high throughput environment and mitigating many of the ethical and methodological constraints present during in vivo experimentation. This work aimed to determine if mechanical loading would offset dexamethasone (DEX) induced skeletal muscle atrophy, in muscle engineered using the C2C12 murine cell line. Mechanical loading successfully offset myotube atrophy and functional degeneration associated with DEX regardless of whether the loading occurred before or after 24 h of DEX treatment. Furthermore, mechanical load prevented increases in MuRF-1 and MAFbx mRNA expression, critical regulators of muscle atrophy. Overall, we demonstrate the application of tissue engineered muscle to study skeletal muscle health and disease, offering great potential for future use to better understand treatment modalities for skeletal muscle atrophy.</p>","PeriodicalId":16422,"journal":{"name":"Journal of Muscle Research and Cell Motility","volume":"42 2","pages":"149-159"},"PeriodicalIF":1.8,"publicationDate":"2021-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8332579/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38401217","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}