Journal articles on the topic 'Myotendinous junction (MTJ)'
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1
Bao, Z. Z., M. Lakonishok, S. Kaufman, and A. F. Horwitz. "Alpha 7 beta 1 integrin is a component of the myotendinous junction on skeletal muscle." Journal of Cell Science 106, no. 2 (October 1, 1993): 579–89. http://dx.doi.org/10.1242/jcs.106.2.579.
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Immunization against a 70 kDa band that co-purifies with skeletal muscle integrins has resulted in an antibody directed against the avain alpha 7 integrin subunit. The specificity of the antibody was established by patterns of tissue staining and cross-reactivity with antibodies directed against the cytoplasmic domain of the rat alpha 7 cytoplasmic domain. On sections of adult skeletal muscle the alpha 7 integrin was enriched in the myotendinous junction (MTJ). This localization was unique as neither the alpha 1, alpha 3, alpha 5, alpha 6 and alpha v subunit localizes in the myotendinous junction. The distribution of the alpha 7 subunit in the MTJ was examined during embryonic development. alpha 7 expression in the junction is first apparent around embryo day 14 and is almost exclusively at the developing MTJ at this stage. alpha 3 is expressed with distinctive punctate staining around the junctional area in earlier embryos (11-day). The time of appearance of the alpha 7 subunit in the MTJ correlates with the insertion of myofibrils into subsarcolemmal densities and folding of the junctional membrane, suggesting a role of the alpha 7 integrin in this process. Vinculin is present throughout development of the myotendinous junction, suggesting that the alpha 7 integrin recognizes a preformed cytoskeletal structure. The presence of the alpha 7 subunit in the myotendinous junction and the alpha 5 subunit in the adhesion plaque demonstrates a molecular difference between these two adherens junctions. It also points to possible origins of junctional specificity on muscle. Differences between these two junctions were developed further using an antibody against phosphotyrosine (PY20). Phosphotyrosine is thought to participate in the organization and stabilization of adhesions. The focal adhesion and the neuromuscular junction, but not the MTJ, contained proteins phosphorylated on tyrosine.
2
Yan, Ruojin, Hong Zhang, Yuanzhu Ma, Ruifu Lin, Bo Zhou, Tao Zhang, Chunmei Fan, et al. "Discovery of Muscle-Tendon Progenitor Subpopulation in Human Myotendinous Junction at Single-Cell Resolution." Research 2022 (September 29, 2022): 1–16. http://dx.doi.org/10.34133/2022/9760390.
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The myotendinous junction (MTJ) is a complex and special anatomical area that connects muscles and tendons, and it is also the key to repairing tendons. Nevertheless, the anatomical structure and connection structure of MTJ, the cluster and distribution of cells, and which cells are involved in repairing the tissue are still unclear. Here, we analyzed the cell subtype distribution and function of human MTJ at single-cell level. We identified four main subtypes, including stem cell, muscle, tendon, and muscle-tendon progenitor cells (MTP). The MTP subpopulation, which remains the characteristics of stem cells and also expresses muscle and tendon marker genes simultaneously, may have the potential for bidirectional differentiation. We also found the muscle-tendon progenitor cells were distributed in the shape of a transparent goblet; muscle cells first connect to the MTP and then to the tendon. And after being transplanted in the MTJ injury model, MTP exhibited strong regenerative capability. Finally, we also demonstrated the importance of mTOR signaling for MTP maintenance by in vitro addition of rapamycin and in vivo validation using mTOR-ko mice. Our research conducted a comprehensive analysis of the heterogeneity of myotendinous junction, discovered a special cluster called MTP, provided new insights into the biological significance of myotendinous junction, and laid the foundation for future research on myotendinous junction regeneration and restoration.
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Zhou, Guang-Quan, Yi Zhang, Ruo-Li Wang, Ping Zhou, Yong-Ping Zheng, Olga Tarassova, Anton Arndt, and Qiang Chen. "Automatic Myotendinous Junction Tracking in Ultrasound Images with Phase-Based Segmentation." BioMed Research International 2018 (2018): 1–12. http://dx.doi.org/10.1155/2018/3697835.
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Displacement of the myotendinous junction (MTJ) obtained by ultrasound imaging is crucial to quantify the interactive length changes of muscles and tendons for understanding the mechanics and pathological conditions of the muscle-tendon unit during motion. However, the lack of a reliable automatic measurement method restricts its application in human motion analysis. This paper presents an automated measurement of MTJ displacement using prior knowledge on tendinous tissues and MTJ, precluding the influence of nontendinous components on the estimation of MTJ displacement. It is based on the perception of tendinous features from musculoskeletal ultrasound images using Radon transform and thresholding methods, with information about the symmetric measures obtained from phase congruency. The displacement of MTJ is achieved by tracking manually marked points on tendinous tissues with the Lucas-Kanade optical flow algorithm applied over the segmented MTJ region. The performance of this method was evaluated on ultrasound images of the gastrocnemius obtained from 10 healthy subjects (26.0±2.9 years of age). Waveform similarity between the manual and automatic measurements was assessed by calculating the overall similarity with the coefficient of multiple correlation (CMC). In vivo experiments demonstrated that MTJ tracking with the proposed method (CMC = 0.97±0.02) was more consistent with the manual measurements than existing optical flow tracking methods (CMC = 0.79±0.11). This study demonstrated that the proposed method was robust to the interference of nontendinous components, resulting in a more reliable measurement of MTJ displacement, which may facilitate further research and applications related to the architectural change of muscles and tendons.
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Pimentel Neto, Jurandyr, Lara Caetano Rocha-Braga, Carolina dos Santos Jacob, André Neri Tomiate, and Adriano Polican Ciena. "Myotendinous Junction: Exercise Protocols Can Positively Influence Their Development in Rats." Biomedicines 10, no. 2 (February 18, 2022): 480. http://dx.doi.org/10.3390/biomedicines10020480.
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The myotendinous junction (MTJ) is an interface that different stimuli alter their morphology. One of the main stimuli to promote alterations in the MTJ morphology is physical exercise. The present study aimed to investigate the morphology and molecular MTJ adaptations of biceps brachii muscle in adult Wistar rats submitted to different ladder-based protocols. Forty Wistar rats (90 days old) were divided into four groups: Sedentary (S), Climbing (C), Overload Climbing (OC), Climbing, and Overload Climbing (COC). The results of light microscopy demonstrated the cell and collagen tissue reorganization in the experimental groups. The sarcomeres lengths of different regions showed a particular development according to the specific protocols. The sarcoplasmic invaginations and evaginations demonstrated positive increases that promoted the myotendinous interface development. In the extracellular matrix, the structures presented an increase principally in the COC group. Finally, the immunofluorescence analysis showed the telocytes disposition adjacent to the MTJ region in all experimental groups, revealing their network organization. Thus, we concluded that the different protocols contributed to the morphological adaptations with beneficial effects in distinct ways of tissue and cellular development and can be used as a model for MTJ remodeling to future proteomic and genetic analysis.
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Jakobsen, Jens R., Peter Schjerling, Rene B. Svensson, Rikke Buhl, Helena Carstensen, Manuel Koch, Michael R. Krogsgaard, Michael Kjær, and Abigail L. Mackey. "RNA sequencing and immunofluorescence of the myotendinous junction of mature horses and humans." American Journal of Physiology-Cell Physiology 321, no. 3 (September 1, 2021): C453—C470. http://dx.doi.org/10.1152/ajpcell.00218.2021.
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The myotendinous junction (MTJ) is a specialized interface for transmitting high forces between the muscle and tendon and yet the MTJ is a common site of strain injury with a high recurrence rate. The aim of this study was to identify previously unknown MTJ components in mature animals and humans. Samples were obtained from the superficial digital flexor (SDF) muscle-tendon interface of 20 horses, and the tissue was separated through a sequential cryosectioning approach into muscle, MTJ (muscle tissue enriched in myofiber tips attached to the tendon), and tendon fractions. RT-PCR was performed for genes known to be expressed in the three tissue fractions and t-distributed stochastic neighbor embedding (t-SNE) plots were used to select the muscle, MTJ, and tendon samples from five horses for RNA sequencing. The expression of previously known and unknown genes identified through RNA sequencing was studied by immunofluorescence on human hamstring MTJ tissue. The main finding was that RNA sequencing identified the expression of a panel of 61 genes enriched at the MTJ. Of these, 48 genes were novel for the MTJ and 13 genes had been reported to be associated with the MTJ in earlier studies. The expression of known [COL22A1 (collagen XXII), NCAM (neural cell adhesion molecule), POSTN (periostin), NES (nestin), OSTN (musclin/osteocrin)] and previously undescribed [MNS1 (meiosis-specific nuclear structural protein 1), and LCT (lactase)] MTJ genes was confirmed at the protein level by immunofluorescence on tissue sections of human MTJ. In conclusion, in muscle-tendon interface tissue enriched with myofiber tips, we identified the expression of previously unknown MTJ genes representing diverse biological processes, which may be important in the maintenance of the specialized MTJ.
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Jacob, Carolina dos S., Gabriela K. Barbosa, Mariana P. Rodrigues, Jurandyr Pimentel Neto, Lara C. Rocha-Braga, Camilla G. de Oliveira, Marucia Chacur, and Adriano P. Ciena. "Ultrastructural and Molecular Development of the Myotendinous Junction Triggered by Stretching Prior to Resistance Exercise." Microscopy and Microanalysis 28, no. 2 (March 8, 2022): 537–42. http://dx.doi.org/10.1017/s1431927622000186.
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The myotendinous junction (MTJ) is a highly specialized region of the locomotor apparatus. Here, we investigated the ultrastructural and molecular effects in the MTJ region after static stretching prior to the ladder-based resistance training. Thirty-two male, 60-day old Wistar rats were divided into four groups: Sedentary, Resistance Training, Stretching, and Stretching-Resistance Training. The gastrocnemius muscle was processed for transmission electron microscopy techniques and Western blot assay. We observed that the static stretching prior to the ladder-based resistance training increased the MTJ components, the fibroblast growth factor (FGF)-2 and FGF-6 protein expression. Also, we demonstrated the lower transforming growth factor expression and no difference in the lysyl oxidase expression after combined training. The MTJ alterations in response to combined training demonstrate adaptive mechanisms which can be used for the prescription or development of methods to reduce or prevent injuries in humans and promote the myotendinous interface benefit.
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Pedrosa-Domellöf, Fatima, Carl-Fredrik Tiger, Ismo Virtanen, Lars-Eric Thornell, and Donald Gullberg. "Laminin Chains in Developing and Adult Human Myotendinous Junctions." Journal of Histochemistry & Cytochemistry 48, no. 2 (February 2000): 201–9. http://dx.doi.org/10.1177/002215540004800205.
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In addition to being the specialized site for transmission of force from the muscle to the tendon, the myotendinous junction (MTJ) also plays an important role in muscle splitting during morphogenesis. An early event in the formation of the MTJ is a regional deposition of basement membranes. We used immunocytochemistry to investigate the distribution of laminin chains during the development of MTJs in human limb muscle at 8-22 weeks of gestation (wg) and in adult MTJs. We used polyclonal antibodies and a new monoclonal antibody (MAb) against the human laminin α1 G4/G5 domains. At 8-10 wg, laminin α1 and laminin α5 chains were specifically localized to the MTJ. Laminin α1 chain remained restricted to the MTJ at 22 wg as the laminin β2 chain had appeared, whereas the laminin α5 chain became deposited along the entire length of the myotubes from 12 wg. In the adult MTJ, only vestigial amounts of laminin α1 and laminin α5 chains could be detected. On the basis of co-distribution data, we speculate that laminin α1 chain in the forming MTJ undergoes an isoform switch from laminin 1 to laminin 3. Our data indicate a potentially important role for laminin α1 chain in skeletal muscle formation.
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Rocha, Lara Caetano, Gabriela Klein Barbosa, Jurandyr Pimentel Neto, Carolina dos Santos Jacob, Andreas B. Knudsen, Ii-Sei Watanabe, and Adriano Polican Ciena. "Aquatic Training after Joint Immobilization in Rats Promotes Adaptations in Myotendinous Junctions." International Journal of Molecular Sciences 22, no. 13 (June 29, 2021): 6983. http://dx.doi.org/10.3390/ijms22136983.
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The myotendinous junction (MTJ) is the muscle-tendon interface and constitutes an integrated mechanical unit to force transmission. Joint immobilization promotes muscle atrophy via disuse, while physical exercise can be used as an adaptative stimulus. In this study, we aimed to investigate the components of the MTJ and their adaptations and the associated elements triggered with aquatic training after joint immobilization. Forty-four male Wistar rats were divided into sedentary (SD), aquatic training (AT), immobilization (IM), and immobilization/aquatic training (IMAT) groups. The samples were processed to measure fiber area, nuclear fractal dimension, MTJ nuclear density, identification of telocytes, sarcomeres, and MTJ perimeter length. In the AT group, the maintenance of ultrastructure and elements in the MTJ region were observed; the IM group presented muscle atrophy effects with reduced MTJ perimeter; the IMAT group demonstrated that aquatic training after joint immobilization promotes benefits in the muscle fiber area and fractal dimension, in the MTJ region shows longer sarcomeres and MTJ perimeter. We identified the presence of telocytes in the MTJ region in all experimental groups. We concluded that aquatic training is an effective rehabilitation method after joint immobilization due to reduced muscle atrophy and regeneration effects on MTJ in rats.
9
Tidball, J. G., and D. M. Quan. "Reduction in myotendinous junction surface area of rats subjected to 4-day spaceflight." Journal of Applied Physiology 73, no. 1 (July 1, 1992): 59–64. http://dx.doi.org/10.1152/jappl.1992.73.1.59.
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The surface area of myotendinous junctions (MTJs), expressed relative to the cross-sectional area of myofibrils attached to them, was determined using established morphometric techniques in which the digitlike processes of the cell at MTJs are modeled as circular paraboloids. The relative area, called the folding factor, was measured for six rats after a 4-day spaceflight and six control rats maintained in a vivarium under otherwise identical conditions. Spaceflight resulted in a significant reduction in relative MTJ surface area, from 19.7 +/- 2.3 (SD) in control animals to 13.3 +/- 2.5 for animals after spaceflight. Furthermore, space animals displayed increased numbers of fibroblasts enriched in rough endoplasmic reticulum near the MTJ, a greater number of ribosomes and mitochondria within muscle at the MTJ, and increased occurrence of lesions in the connective tissue near the MTJ. The results indicate that spaceflight, possibly through the removal of gravity-associated loading from muscle, causes a modification in MTJ structure and may result in injuries at MTJs after return to normal loading.
10
Dix, D. J., and B. R. Eisenberg. "Myosin mRNA accumulation and myofibrillogenesis at the myotendinous junction of stretched muscle fibers." Journal of Cell Biology 111, no. 5 (November 1, 1990): 1885–94. http://dx.doi.org/10.1083/jcb.111.5.1885.
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Myofiber growth and myofibril assembly at the myotendinous junction (MTJ) of stretch-hypertrophied rabbit skeletal muscle was studied by in situ hybridization, immunofluorescence, and electron microscopy. In situ hybridization identified higher levels of myosin heavy chain (MHC) mRNA at the MTJ of fibers stretched for 4 d. Electron microscopy at the MTJ of these lengthening fibers revealed a large cytoplasmic space devoid of myofibrils, but containing polysomes, sarcoplasmic reticulum and T-membranes, mitochondria, Golgi complexes, and nascent filament assemblies. Tallies from electron micrographs indicate that myofibril assembly in stretched fibers followed a set sequence of events. (a) In stretched fiber ends almost the entire sarcolemmal membrane was electron dense but only a portion had attached myofibrils. Vinculin, detected by immunofluorescence, was greatly increased at the MTJ membrane of stretched muscles. (b) Thin filaments were anchored to the sarcolemma at the electron dense sites. (c) Thick filaments associated with these thin filaments in an unregistered manner. (d) Z-bodies splice into thin filaments and subsequently thin and thick filaments fall into sarcomeric register. Thus, the MTJ is a site of mRNA accumulation which sets up regional protein synthesis and myofibril assembly. Stretched muscles also lengthen by the addition of myotubes at their ends. After 6 d of stretch these myotubes make up the majority of fibers at the muscle ends. Essentially all these myotubes repeat the developmental program of primary myotubes and express slow MHC. MHC mRNA distribution in myotubes is disorganized as is the distribution of their myofibrils.
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Chen, Q., R. Sealock, and H. B. Peng. "A protein homologous to the Torpedo postsynaptic 58K protein is present at the myotendinous junction." Journal of Cell Biology 110, no. 6 (June 1, 1990): 2061–71. http://dx.doi.org/10.1083/jcb.110.6.2061.
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The 58K protein is a peripheral membrane protein enriched in the acetylcholine receptor (AChR)-rich postsynaptic membrane of Torpedo electric organ. Because of its coexistence with AChRs in the postsynaptic membrane in both electrocytes and skeletal muscle, it is thought to be involved in the formation and maintenance of AChR clusters. Using an mAb against the 58K protein of Torpedo electric organ, we have identified a single protein band in SDS-PAGE analysis of Xenopus myotomal muscle with an apparent molecular mass of 48 kD. With this antibody, the distribution of this protein was examined in the myotomal muscle fibers with immunofluorescence techniques. We found that the 48K protein is concentrated at the myotendinous junctions (MTJs) of these muscle fibers. The MTJ is also enriched in talin and vinculin. By double labeling muscle fibers with antibodies against talin and the 48K protein, these two proteins were found to colocalize at the membrane invaginations of the MTJ. In cultured myotomal muscle cells, the 48K protein and talin are also colocalized at sites of membrane-myofibril interaction. The 48K protein is, however, not found at focal adhesion sites in nonmuscle cells, which are enriched in talin. These data suggest that the 48K protein is specifically involved in the interaction of myofibrillar actin filaments with the plasma membrane at the MTJ. In addition to the MTJ localization, 48K protein is also present at AChR clusters both in vivo and in vitro. Thus, this protein is shared by both the MTJ and the neuromuscular junction.
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Miyamoto-Mikami, Eri, Hiroshi Kumagai, Naoki Kikuchi, Nobuhiro Kamiya, Naokazu Miyamoto, and Noriyuki Fuku. "eQTL variants in COL22A1 are associated with muscle injury in athletes." Physiological Genomics 52, no. 12 (December 1, 2020): 588–89. http://dx.doi.org/10.1152/physiolgenomics.00115.2020.
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The myotendinous junction (MTJ) is at high risk of muscle injury, and collagen XXII is strictly expressed at tissue junctions, specifically at the MTJ. We investigated the hypothesis that single-nucleotide polymorphisms (SNPs) related to collagen type XXII α-1 chain gene ( COL22A1) mRNA expression are associated with susceptibility to muscle injury in athletes. History of muscle injury was assessed in 3,320 Japanese athletes using a questionnaire, and two expression quantitative trait loci (eQTL) SNPs for COL22A1 (rs11784270 A/C and rs6577958 T/C) were analyzed using the TaqMan SNP Genotyping Assay. rs11784270 [odds ratio (OR) = 1.80, 95% confidence interval (CI) = 1.27–2.62, P = 0.0006] and rs6577958 (OR = 1.45, 95% CI = 1.10–1.94, P = 0.0083) were significantly associated with muscle injury under A and T allele additive genetic models, respectively. These results suggest that the expression level of COL22A1 at the MTJ influences muscle injury risk in athletes.
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Matchett, Emma F., Shuaijin Wang, and Bryan D. Crawford. "Paralogues of Mmp11 and Timp4 Interact during the Development of the Myotendinous Junction in the Zebrafish Embryo." Journal of Developmental Biology 7, no. 4 (December 3, 2019): 22. http://dx.doi.org/10.3390/jdb7040022.
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The extracellular matrix (ECM) of the myotendinous junction (MTJ) undergoes dramatic physical and biochemical remodeling during the first 48 h of development in zebrafish, transforming from a rectangular fibronectin-dominated somite boundary to a chevron-shaped laminin-dominated MTJ. Matrix metalloproteinase 11 (Mmp11, a.k.a. Stromelysin-3) is both necessary and sufficient for the removal of fibronectin at the MTJ, but whether this protease acts directly on fibronectin and how its activity is regulated remain unknown. Using immunofluorescence, we show that both paralogues of Mmp11 accumulate at the MTJ during this time period, but with Mmp11a present early and later replaced by Mmp11b. Moreover, Mmp11a also accumulates intracellularly, associated with the Z-discs of sarcomeres within skeletal muscle cells. Using the epitope-mediated MMP activation (EMMA) assay, we show that despite having a weaker paired basic amino acid motif in its propeptide than Mmp11b, Mmp11a is activated by furin, but may also be activated by other mechanisms intracellularly. One or both paralogues of tissue inhibitors of metalloproteinase-4 (Timp4) are also present at the MTJ throughout this process, and yeast two-hybrid assays reveal distinct and specific interactions between various domains of these proteins. We propose a model in which Mmp11a activity is modulated (but not inhibited) by Timp4 during early MTJ remodeling, followed by a phase in which Mmp11b activity is both inhibited and spatially constrained by Timp4 in order to maintain the structural integrity of the mature MTJ.
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Joannas, German, Leandro Casola, Guillermo Arrondo, Daniel Niño Gomez, and Santiago Labbate. "V-Y advancement flap for repair of neglected injuries of the Achilles tendon using 2 mini-incisions." Journal of the Foot & Ankle 14, no. 2 (August 30, 2020): 123–25. http://dx.doi.org/10.30795/jfootankle.2020.v14.1186.
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Objective: To find a safe repair site for a proximal mini-incision to expose the fascia at the level of the gastrocnemius medialis (GM) myotendinous junction (MTJ). Methods: Seventeen anatomic specimens of popliteal fossa, leg, and foot fixed in formalin were dissected, and the perpendicular distance from the apex of the medial malleolus to the GM MTJ was measured. Results: The minimum and maximum perpendicular distances from the apex of the medial malleolus to the GM MTJ were 14.00cm and 20.5cm, respectively. Average distance was 16.56cm. Conclusion: We were able to establish a constant value and the average GM MTJ height, which allows for V-Y lengthening through 2 mini-incisions. In reviewing the literature, there was no description of the approaches proposed in this study. Level of Evidence VI; Therapeutic Studies; Case Series.Achilles tendon/surgery
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Korkmaz, Yüksel, Franz J. Klinz, Mehrnoush Moghbeli, Klaus Addicks, Wolfgang H. M. Raab, and Wilhelm Bloch. "The Masticatory Contractile Load Induced Expression and Activation of Akt1/PKBαin Muscle Fibers at the Myotendinous Junction within Muscle-Tendon-Bone Unit." Journal of Biomedicine and Biotechnology 2010 (2010): 1–8. http://dx.doi.org/10.1155/2010/163203.
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The cell specific detection of enzyme activation in response to the physiological contractile load within muscle-tendon-bone unit is essential for understanding of the mechanical forces transmission from muscle cells via tendon to the bone. The hypothesis that the physiological mechanical loading regulates activation of Akt1/PKBαat Thr308 and at Ser473 in muscle fibers within muscle-tendon-bone unit was tested using quantitative immunohistochemistry, confocal double fluorescence analysis, and immunoblot analysis. In comparison to the staining intensities in peripheral regions of the muscle fibers, Akt1/PKBαwas detected with a higher staining intensity in muscle fibers at the myotendinous junction (MTJ) areas. In muscle fibers at the MTJ areas, Akt1/PKBαis dually phosphorylated at Thr308 and Ser473. The immunohistochemical results were confirmed by immunoblot analysis. We conclude that contractile load generated by masticatory muscles induces local domain-dependent expression of Akt1/PKBαas well as activation by dually phosphorylation at Thr308 and Ser473 in muscle fibers at the MTJ areas within muscle-tendon-bone unit.
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Peng, H. B., and Q. Chen. "Induction of dystrophin localization in cultured Xenopus muscle cells by latex beads." Journal of Cell Science 103, no. 2 (October 1, 1992): 551–63. http://dx.doi.org/10.1242/jcs.103.2.551.
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The distribution of dystrophin in Xenopus myotomal muscle cells was examined in conventional and confocal immunofluorescence microscopy. By labeling dissociated single muscle fibers with a monoclonal or a polyclonal antibody against dystrophin, we found that dystrophin is ten times more concentrated at the myotendinous junction (MTJ) than at the extrajunctional sarcolemma. At the MTJ, dystrophin lines the membrane invaginations where myofibrils attach to the membrane. It is colocalized with talin, but is not related to the distribution of acetylcholine receptors (AChRs) which are clustered at the postsynaptic membrane in the vicinity of the MTJ in these fibers. We found that the localization of dystrophin can be induced in cultured Xenopus myotomal muscle cells by treating them with polystyrene latex beads. Dystrophin is discretely localized at the bead-muscle contacts. With electron microscopy, a sarcolemma specialization with all the salient features of the MTJ, including basal lamina-lined membrane invaginations along which myofibrils make attachment. Although these beads also induce clustering of AChRs, the patterns of dystrophin and AChR localization are distinct. The appearance of dystrophin at the bead-contacted sarcolemma is coincident with the development of the membrane invaginations. This, together with its concentration along membrane invaginations at the MTJ in vivo, suggests a role for dystrophin in the formation of this junctional specialization. Since the signal for MTJ development can be presented to cultured muscle cells in a temporally and spatially controlled manner by beads, this system offers a simple model for analyzing the mechanism of this sarcolemma specialization.
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Feng, Han-Zhong, Qinchuan Wang, Rebecca S. Reiter, Jenny L. C. Lin, Jim J. C. Lin, and J. P. Jin. "Localization and function of Xinα in mouse skeletal muscle." American Journal of Physiology-Cell Physiology 304, no. 10 (May 15, 2013): C1002—C1012. http://dx.doi.org/10.1152/ajpcell.00005.2013.
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The Xin repeat-containing proteins were originally found in the intercalated discs of cardiac muscle with implicated roles in cardiac development and function. A pair of paralogous genes, Xinα ( Xirp1) and Xinβ ( Xirp2), is present in mammals. Ablation of the mouse Xinα ( mXinα) did not affect heart development but caused late-onset adulthood cardiac hypertrophy and cardiomyopathy with conductive defects. Both mXinα and mXinβ are also found in the myotendinous junction (MTJ) of skeletal muscle. Here we investigated the structural and functional significance of mXinα in skeletal muscle. In addition to MTJ and the contact sites between muscle and perimysium, mXinα but not mXinβ was found in the blood vessel walls, whereas both proteins were absent in neuromuscular junctions and nerve fascicles. Coimmunoprecipitation suggested association of mXinα with talin, vinculin, and filamin, but not β-catenin, in adult skeletal muscle, consistent with our previous report of colocalization of mXinα with vinculin. Loss of mXinα in mXinα-null mice had subtle effects on the MTJ structure and the levels of several MTJ components. Diaphragm muscle of mXinα-null mice showed hypertrophy. Compared with wild-type controls, mouse extensor digitorum longus (EDL) muscle lacking mXinα exhibited no overt change in contractile and relaxation velocities or maximum force development but better tolerance to fatigue. Loaded fatigue contractions generated stretch injury in wild-type EDL muscle as indicated by a fragmentation of troponin T. This effect was blunted in mXinα-null EDL muscle. The results suggest that mXinα play a role in MTJ conductance of contractile and stretching forces.
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Riccetti, Manon, Jules Opplert, Joao L. Q. Durigan, Carole Cometti, and Nicolas Babault. "Acute Static Stretching Results in Muscle-Specific Alterations amongst the Hamstring Muscles." Sports 8, no. 9 (August 30, 2020): 119. http://dx.doi.org/10.3390/sports8090119.
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This study aimed to explore the acute effects of static stretching on the musculotendinous properties of two hamstring muscles. Twelve male volunteers underwent two testing sessions. One session was dedicated to the evaluation of the semitendinosus muscle before (PRE) and after (POST) static stretching (five sets of 30-s stretching), and the other session similarly explored the long head of biceps femoris muscle. In addition to the displacement of the myotendinous junction (MTJ), passive torque and maximal voluntary isometric torque (MVIT) were evaluated. MVIT (−8.3 ± 10.2%, p = 0.0036, d = 0.497) and passive torque (−28.4 ± 16.9%, p = 0.0003, d = 1.017) were significantly decreased POST stretching. PRE stretching, MTJ displacement was significantly greater for semitendinosus muscle than biceps femoris muscle (27.0 ± 5.2 vs. 18.6 ± 3.6, p = 0.0011, d = 1.975). After the stretching procedure, greater MTJ displacement relative changes were observed for biceps femoris muscle as compared to semitendinosus muscle (22.4 ± 31.6 vs. −8.4 ± 17.9, p = 0.0167, d = 1.252). Because of the smaller MTJ displacement PRE stretching and greater alteration POST stretching in biceps femoris muscles, the present study demonstrated muscle-specific acute responses of hamstring muscles during stretching. Although stretching acutely impairs torque production, the passive torque reduction and alteration of MTJ displacement might impact hamstring injury prevention.
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Coffey, Elizabeth C., Mary Astumian, Sarah S. Alrowaished, Claire Schaffer, and Clarissa A. Henry. "Lysosomal Function Impacts the Skeletal Muscle Extracellular Matrix." Journal of Developmental Biology 9, no. 4 (November 23, 2021): 52. http://dx.doi.org/10.3390/jdb9040052.
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Muscle development and homeostasis are critical for normal muscle function. A key aspect of muscle physiology during development, growth, and homeostasis is modulation of protein turnover, the balance between synthesis and degradation of muscle proteins. Protein degradation depends upon lysosomal pH, generated and maintained by proton pumps. Sphingolipid transporter 1 (spns1), a highly conserved gene encoding a putative late endosome/lysosome carbohydrate/H+ symporter, plays a pivotal role in maintaining optimal lysosomal pH and spns1−/− mutants undergo premature senescence. However, the impact of dysregulated lysosomal pH on muscle development and homeostasis is not well understood. We found that muscle development proceeds normally in spns1−/− mutants prior to the onset of muscle degeneration. Dysregulation of the extracellular matrix (ECM) at the myotendinous junction (MTJ) coincided with the onset of muscle degeneration in spns1−/− mutants. Expression of the ECM proteins laminin 111 and MMP-9 was upregulated. Upregulation of laminin 111 mitigated the severity of muscle degeneration, as inhibition of adhesion to laminin 111 exacerbated muscle degeneration in spns1−/− mutants. MMP-9 upregulation was induced by tnfsf12 signaling, but abrogation of MMP-9 did not impact muscle degeneration in spns1−/− mutants. Taken together, these data indicate that dysregulated lysosomal pH impacts expression of ECM proteins at the myotendinous junction.
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Hakim, Chady H., Robert W. Grange, and Dongsheng Duan. "The passive mechanical properties of the extensor digitorum longus muscle are compromised in 2- to 20-mo-old mdx mice." Journal of Applied Physiology 110, no. 6 (June 2011): 1656–63. http://dx.doi.org/10.1152/japplphysiol.01425.2010.
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Muscle rigidity and myotendinous junction (MTJ) deficiency contribute to immobilization in Duchenne muscular dystrophy (DMD), a lethal disease caused by the absence of dystrophin. However, little is known about the muscle passive properties and MTJ strength in a diseased muscle. Here, we hypothesize that dystrophin-deficient muscle pathology renders skeletal muscle stiffer and MTJ weaker. To test our hypothesis, we examined the passive properties of an intact noncontracting muscle-tendon unit in mdx mice, a mouse model for DMD. The extensor digitorum longus (EDL) muscle-tendon preparations of 2-, 6-, 14-, and 20-mo-old mdx and normal control mice were strained stepwisely from 110% to 160% of the muscle optimal length. The stress-strain response and failure position were analyzed. In support of our hypothesis, the mdx EDL preparation consistently developed higher stress before muscle failure. Postfailure stresses decreased dramatically in mdx but not normal preparations. Further, mdx showed a significantly faster stress relaxation rate. Consistent with stress-strain assay results, we observed significantly higher fibrosis in mdx muscle. In 2- and 6-mo-old mdx and 20-mo-old BL10 mice failure occurred within the muscle (2- to 14-mo-old BL10 preparations did not fail). Interestingly, in ≥14-mo-old mdx mice the failure site shifted toward the MTJ. Electron microscopy revealed substantial MTJ degeneration in aged but not young mdx mice. In summary, our results suggest that the passive properties of the EDL muscle and the strength of MTJ are compromised in mdx in an age-dependent manner. These findings offer new insights in studying DMD pathogenesis and developing novel therapies.
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Boppart, Marni D., Sonja E. Volker, Nicole Alexander, Dean J. Burkin, and Stephen J. Kaufman. "Exercise promotes α7 integrin gene transcription and protection of skeletal muscle." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 295, no. 5 (November 2008): R1623—R1630. http://dx.doi.org/10.1152/ajpregu.00089.2008.
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The α7β1 integrin is increased in skeletal muscle in response to injury-producing exercise, and transgenic overexpression of this integrin in mice protects against exercise-induced muscle damage. The present study investigates whether the increase in the α7β1 integrin observed in wild-type mice in response to exercise is due to transcriptional regulation and examines whether mobilization of the integrin at the myotendinous junction (MTJ) is a key determinant in its protection against damage. A single bout of downhill running exercise selectively increased transcription of the α7 integrin gene in 5-wk-old wild-type mice 3 h postexercise, and an increased α7 chain was detected in muscle sarcolemma adjacent to tendinous tissue immediately following exercise. The α7B, but not α7A isoform, was found concentrated and colocalized with tenascin-C in muscle fibers lining the MTJ. To further validate the importance of the integrin in the protection against muscle damage following exercise, muscle injury was quantified in α7−/−mice. Muscle damage was extensive in α7−/−mice in response to both a single and repeated bouts of exercise and was largely restricted to areas of high MTJ concentration and high mechanical force near the Achilles tendon. These results suggest that exercise-induced muscle injury selectively increases transcription of the α7 integrin gene and promotes a rapid change in the α7β integrin at the MTJ. These combined molecular and cellular alterations are likely responsible for integrin-mediated attenuation of exercise-induced muscle damage.
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Lau, Wing Yin, Anthony J. Blazevich, Michael J. Newton, Sam Shi Xuan Wu, and Kazunori Nosaka. "Reduced muscle lengthening during eccentric contractions as a mechanism underpinning the repeated-bout effect." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 308, no. 10 (May 15, 2015): R879—R886. http://dx.doi.org/10.1152/ajpregu.00338.2014.
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This study investigated biceps brachii distal myotendinous junction (MTJ) displacement during maximal eccentric elbow flexor contractions to test the hypothesis that muscle length change would be smaller (less MTJ displacement) during the second than the first exercise bout. Ten untrained men performed two eccentric exercise bouts (ECC1 and ECC2) with the same arm consisting of 10 sets of six maximal isokinetic (60°/s) eccentric elbow flexor contractions separated by 4 wk. Biceps brachii distal MTJ displacement was assessed using B-mode ultrasonography, and changes in the displacement (muscle length change) from the start to the end of each contraction during each set and over 10 sets were compared between bouts by two-way repeated-measures ANOVA. Several indirect muscle damage markers were also measured and compared between bouts by two-way repeated-measures ANOVA. The magnitude of MTJ displacement (average of six contractions) increased from set 1 (8.2 ± 4.7 mm) to set 10 (16.4 ± 4.7 mm) during ECC1 ( P < 0.05), but no significant changes over sets were evident during ECC2 ( set 1: 8.5 ± 4.0 mm; set 10: 9.3 ± 3.1 mm). Changes in maximal voluntary isometric contraction strength, range of motion, muscle thickness, ultrasound echo intensity, serum creatine kinase activity, and muscle soreness (visual analog scale) were smaller ( P < 0.05) following ECC2 than ECC1, showing less damage in the repeated bout. These results indicate that the magnitude of muscle lengthening was less during the second than the first eccentric exercise bout, which appears to be a mechanism underpinning the repeated-bout effect.
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Crosbie, Rachelle H., Connie S. Lebakken, Kathleen H. Holt, David P. Venzke, Volker Straub, Jane C. Lee, R. Mark Grady, Jeffery S. Chamberlain, Joshua R. Sanes, and Kevin P. Campbell. "Membrane Targeting and Stabilization of Sarcospan Is Mediated by the Sarcoglycan Subcomplex." Journal of Cell Biology 145, no. 1 (April 5, 1999): 153–65. http://dx.doi.org/10.1083/jcb.145.1.153.
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The dystrophin–glycoprotein complex (DGC) is a multisubunit complex that spans the muscle plasma membrane and forms a link between the F-actin cytoskeleton and the extracellular matrix. The proteins of the DGC are structurally organized into distinct subcomplexes, and genetic mutations in many individual components are manifested as muscular dystrophy. We recently identified a unique tetraspan-like dystrophin-associated protein, which we have named sarcospan (SPN) for its multiple sarcolemma spanning domains (Crosbie, R.H., J. Heighway, D.P. Venzke, J.C. Lee, and K.P. Campbell. 1997. J. Biol. Chem. 272:31221–31224). To probe molecular associations of SPN within the DGC, we investigated SPN expression in normal muscle as a baseline for comparison to SPN's expression in animal models of muscular dystrophy. We show that, in addition to its sarcolemma localization, SPN is enriched at the myotendinous junction (MTJ) and neuromuscular junction (NMJ), where it is a component of both the dystrophin– and utrophin–glycoprotein complexes. We demonstrate that SPN is preferentially associated with the sarcoglycan (SG) subcomplex, and this interaction is critical for stable localization of SPN to the sarcolemma, NMJ, and MTJ. Our experiments indicate that assembly of the SG subcomplex is a prerequisite for targeting SPN to the sarcolemma. In addition, the SG– SPN subcomplex functions to stabilize α-dystroglycan to the muscle plasma membrane. Taken together, our data provide important information about assembly and function of the SG–SPN subcomplex.
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Rochlin, M. W., Q. M. Chen, M. Tobler, C. E. Turner, K. Burridge, and H. B. Peng. "The relationship between talin and acetylcholine receptor clusters in Xenopus muscle cells." Journal of Cell Science 92, no. 3 (March 1, 1989): 461–72. http://dx.doi.org/10.1242/jcs.92.3.461.
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Talin is involved in mediating the cytoskeleton-extracellular matrix interaction at focal contacts in cultured fibroblasts. Recently this protein has been localized at both the myotendinous junction (MTJ) and the neuromuscular junction (NMJ) in skeletal muscle. At the MTJ, talin may mediate the insertion of myofibrils into the plasma membrane, thus serving a function similar to that seen at focal contacts. However, the function of talin at the NMJ is unknown. In this study, we examined its distribution at both mature and developing acetylcholine receptor (AChR) clusters in Xenopus muscle cells both in vivo and in vitro with immunofluorescence. At the NMJs of both myotomal and submaxillaris muscles, talin was absent from the AChR clusters. In cultured myotomal muscle cells, it was absent from 40% of both the nerve-associated AChR patches and the spontaneously formed AChR clusters located on the top surface of the cells. We therefore conclude that this protein is not essential for maintenance of AChR clusters at the NMJ. In addition to MTJs, talin was invariably associated with AChR clusters induced by polyornithine-coated beads, and, to a large extent, with spontaneously formed clusters on the ventral side of cultured cells. A common feature of these talin-positive domains is the deep membrane infoldings, where bundles of actin filaments are inserted into the membrane. Thus, talin may be involved in the formation and maintenance of these structures. The deep membrane infoldings, though prominent at most NMJs, are absent from the two muscles under study in vivo. Our work thus suggests that the postjunctional membrane at the NMJ is heterogeneous, consisting of an AChR cluster domain and, often but not always, a domain for proteins involved in cytoskeleton-membrane linkage as exemplified by talin.
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McDonald, K. A., M. Lakonishok, and A. F. Horwitz. "Alpha v and alpha 3 integrin subunits are associated with myofibrils during myofibrillogenesis." Journal of Cell Science 108, no. 7 (July 1, 1995): 2573–81. http://dx.doi.org/10.1242/jcs.108.7.2573.
Full textAbstract:
The development of the myofibrillar apparatus in skeletal muscle is a process in which transmembrane linkages with adhesion molecules are implicated. Integrins are one class of transmembrane adhesion receptors which appear to mediate these interactions. Two prominent linkages are at the myotendinous junction (MTJ), which resides at the ends of the cell and connects myofibrils to the tendon, and the costameres, which encircle the girth of the cell and connect the Z-disks to the sarcolemma. In this study we report that the alpha v integrin subunit is a prominent component of the costamere. The alpha v subunit is present initially on developing myotubes in a diffuse staining pattern with some concentration along nascent myofibrils. However, it appears in a striated pattern at the costamere and inconsistently at the M-line following the striation of alpha-actinin and titin but before that of desmin. Its recruitment to preformed striation suggests that it is incorporated into a pre-existing structure. The presence of alpha v in the costamere points to a role in lateral myofibrillar anchorage. In addition, we find that the alpha 3 subunit is transiently associated with myofibrils along portions of their lengths and at their ends during myofibrillogenesis. The alpha 3 subunit staining shows a novel localization and junctional structure. As myofibrils become striated the alpha 3 integrin dissociates from the localized pattern and becomes diffuse. This suggests a possible role in the stabilization of nascent myofibrils prior to striation. Antibody-induced perturbation of adhesion mediated by the integrin beta 1 subunit in developing myotubes inhibits assembly of the sarcomeric architecture.(ABSTRACT TRUNCATED AT 250 WORDS)
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McDonald, K. A., M. Lakonishok, and A. F. Horwitz. "Alpha v and alpha 3 integrin subunits are associated with myofibrils during myofibrillogenesis." Journal of Cell Science 108, no. 3 (March 1, 1995): 975–83. http://dx.doi.org/10.1242/jcs.108.3.975.
Full textAbstract:
The development of the myofibrillar apparatus in skeletal muscle is a process in which transmembrane linkages with adhesion molecules are implicated. Integrins are one class of transmembrane adhesion receptors which appear to mediate these interactions. Two prominent linkages are at the myotendinous junction (MTJ), which residues at the ends of the cell and connects myofibrils to the tendon, and the costameres, which encircle the girth of the cell and connect the Z-disks to the sarcolemma. In this study we report that the alpha v integrin subunit is a prominent component of the costamere. The alpha v subunit is present initially on developing myotubes in a diffuse staining pattern with some concentration along nascent myofibrils. However, it appears in a striated pattern at the costamere and inconsistently at the M-line following the striation of alpha-actinin and titin but before that of desmin. Its recruitment to preformed striation suggests that it is incorporated into a pre-existing structure. The presence of alpha v in the costamere points to a role in lateral myofibrillar anchorage. In addition, we find that the alpha 3 subunit is transiently associated with myofibrils along portions of their lengths and at their ends during myofibrillogenesis. The alpha 3 subunit staining shows a novel localization and junctional structure. As myofibrils become striated the alpha 3 integrin dissociates from the localized pattern and becomes diffuse. This suggests a possible role in the stabilization of nascent myofibrils prior to striation. Antibody-induced perturbation of adhesion mediated by the integrin beta 1 subunit in developing myotubes inhibits assembly of the sarcomeric architecture.(ABSTRACT TRUNCATED AT 250 WORDS)
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Curzi, D., P. Ambrogini, S. Burattini, and E. Falcieri. "Morphogenesis of rat myotendinous junction." Muscle Ligaments and Tendons Journal 03, no. 04 (January 2019): 275. http://dx.doi.org/10.32098/mltj.04.2013.07.
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Panwar, K., D. Lara, M. Trzeciak, and E. G. Huish Jr. "Location of the Flexor Carpi Radialis Myotendinous Junction: a Cadaveric Study." Muscle Ligaments and Tendons Journal 11, no. 04 (November 2021): 756. http://dx.doi.org/10.32098/mltj.04.2021.20.
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Sikes, K. J., K. M. Andrie, A. McConnell, S. Wist, S. Smith, B. Cole, D. D. Frisbie, and K. S. Santangelo. "Clinical and Histologic Manifestations of a Novel Rectus Femoris Myotendinous Junction Injury in Rats." Muscle Ligaments and Tendons Journal 11, no. 04 (November 2021): 600. http://dx.doi.org/10.32098/mltj.04.2021.01.
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Onda, H., D. J. Goldhamer, and R. A. Tassava. "An extracellular matrix molecule of newt and axolotl regenerating limb blastemas and embryonic limb buds: immunological relationship of MT1 antigen with tenascin." Development 108, no. 4 (April 1, 1990): 657–68. http://dx.doi.org/10.1242/dev.108.4.657.
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Several well-characterized extracellular matrix (ECM) components have been localized to the amphibian limb regenerate, but the identification and characterization of novel ECM molecules have received little attention. Here we describe, using mAb MT1 and immunocytochemistry, an ECM molecule expressed during limb regeneration and limb development. In limb stumps, mAb MT1 reactivity was restricted to tendons, myotendinous junctions, granules in the basal layers of epidermis, periosteum (newts) and perichondrium (axolotls). In regenerating limbs, reactivity in the distal limb stump was first detected 5 days and 1 day after amputation of newt and axolotl limbs, respectively. In both species, mAb MT1 recognized what appeared to be an abundant blastema matrix antigen, localized in both thin and thick cords between and sometimes closely associated with blastema cells. Reactivity was generally uniform throughout the blastema except for a particularly thick layer that was present immediately beneath the wound epithelium. During redifferentiation stages, mAb MT1 reactivity persisted among blastema cells and redifferentiating cartilage but was lost proximally in areas of muscle and connective tissue differentiation. During the entire period of embryonic limb development, mAb MT1 reactivity was seen in the ECM of the mesenchyme and in a layer beneath the limb bud ectoderm, similar to its distribution during regeneration. Considerable mAb MT1 reactivity was also associated with the developing somites. The reactivity of mAb MT1 in blastema and limb bud was similar if not identical to that of a polyclonal Ab against tenascin (pAbTN), a large, extracellular matrix glycoprotein implicated in growth control, inductive interactions, and other developmental events. This pAbTN effectively competed against mAb MT1 binding on blastema sections. In immunoblots, both mAb MT1 and pAbTN recognized a very high molecular weight (approximately Mr 1000 × 10(3)) protein in blastema extracts of both newts and axolotls. mAb MT1 immunoprecipitated a protein of Mr 1000K size which reacted to both mAb MT1 and pAbTN in immunoblots. These data show that tenascin is in the matrix of the urodele blastema and limb bud, and suggest that mAb MT1 identifies urodele tenascin.
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Jakobsen, Jens Rithamer, and Michael Rindom Krogsgaard. "The Myotendinous Junction—A Vulnerable Companion in Sports. A Narrative Review." Frontiers in Physiology 12 (March 26, 2021). http://dx.doi.org/10.3389/fphys.2021.635561.
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The incidence of strain injuries continues to be high in many popular sports, especially hamstring strain injuries in football, despite a documented important effect of eccentric exercise to prevent strains. Studies investigating the anatomical properties of these injuries in humans are sparse. The majority of strains are seen at the interface between muscle fibers and tendon: the myotendinous junction (MTJ). It has a unique morphology with a highly folded muscle membrane filled with invaginations of collagen fibrils from the tendon, establishing an increased area of force transmission between muscle and tendon. There is a very high rate of remodeling of the muscle cells approaching the MTJ, but little is known about how the tissue adapts to exercise and which structural changes heavy eccentric exercise may introduce. This review summarizes the current knowledge about the anatomy, composition and adaptability of the MTJ, and discusses reasons why strain injuries can be prevented by eccentric exercise.
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Chen, Ziming, Peilin Chen, Monica Zheng, Junjie Gao, Delin Liu, Allan Wang, Qiujian Zheng, Toby Leys, Andrew Tai, and Minghao Zheng. "Challenges and perspectives of tendon-derived cell therapy for tendinopathy: from bench to bedside." Stem Cell Research & Therapy 13, no. 1 (September 2, 2022). http://dx.doi.org/10.1186/s13287-022-03113-6.
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AbstractTendon is composed of dense fibrous connective tissues, connecting muscle at the myotendinous junction (MTJ) to bone at the enthesis and allowing mechanical force to transmit from muscle to bone. Tendon diseases occur at different zones of the tendon, including enthesis, MTJ and midsubstance of the tendon, due to a variety of environmental and genetic factors which consequently result in different frequencies and recovery rates. Self-healing properties of tendons are limited, and cell therapeutic approaches in which injured tendon tissues are renewed by cell replenishment are highly sought after. Homologous use of individual’s tendon-derived cells, predominantly differentiated tenocytes and tendon-derived stem cells, is emerging as a treatment for tendinopathy through achieving minimal cell manipulation for clinical use. This is the first review summarizing the progress of tendon-derived cell therapy in clinical use and its challenges due to the structural complexity of tendons, heterogeneous composition of extracellular cell matrix and cells and unsuitable cell sources. Further to that, novel future perspectives to improve therapeutic effect in tendon-derived cell therapy based on current basic knowledge are discussed.
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Jacob, Carolina dos Santos, Lara Caetano Rocha, Jurandyr Pimentel Neto, Ii-sei Watanabe, and Adriano Polican Ciena. "Effects of physical training on sarcomere lengths and muscle-tendon interface of the cervical region in an experimental model of menopause." European Journal of Histochemistry 63, no. 3 (August 6, 2019). http://dx.doi.org/10.4081/ejh.2019.3038.
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The aim of this study was to describe the structural and ultrastructural aspects of the myotendinous junction (MTJ) and the proximal and distal sarcomeres of the sternomastoid of aged Wistar rats subjected to an experimental model of menopause and swimming training. A total of 20 female elderly rats were divided into the following four groups (n=5 in each group): sedentary/no-menopausal (SNM), trained/no-menopausal (TNM), sedentary/menopausal (SM), and trained/menopausal (TM). The MTJ samples were dissected and analyzed using transmission electron microscopy. We showed that the TNM Group rats exhibited changes in morphological characteristics as a consequence of physical exercise, which included an increase of 36.60% (P<0.001) in the evagination length of the MTJ and a reduction in the length of the distal (77.38%) (P<0.0001) and proximal (68.15%) (P<0.0001) sarcomeres. The SM Group exhibited a reduction of about 275.93% (P<0.001) in the muscle-tendon interface and in the lengths of distal sarcomeres (55.87%) (P<0.0001) compared with SNM Group. Our results suggest that the swimming training under experimental model of menopause promoted tissue reorganization and increased muscle-tendon interaction with a drastic development in the length and thickness of the sarcoplasmatic invaginations and evaginations. In addition, the sarcomeres exhibited different lengths and a reduction in both groups subjected to swimming training.
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Kharazi, Mohamadreza, Sebastian Bohm, Christos Theodorakis, Falk Mersmann, and Adamantios Arampatzis. "Quantifying mechanical loading and elastic strain energy of the human Achilles tendon during walking and running." Scientific Reports 11, no. 1 (March 12, 2021). http://dx.doi.org/10.1038/s41598-021-84847-w.
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AbstractThe purpose of the current study was to assess in vivo Achilles tendon (AT) mechanical loading and strain energy during locomotion. We measured AT length considering its curve-path shape. Eleven participants walked at 1.4 m/s and ran at 2.5 m/s and 3.5 m/s on a treadmill. The AT length was defined as the distance between its origin at the gastrocnemius medialis myotendinous junction (MTJ) and the calcaneal insertion. The MTJ was tracked using ultrasonography and projected to the reconstructed skin surface to account for its misalignment. Skin-to-bone displacements were assessed during a passive rotation (5°/s) of the ankle joint. Force and strain energy of the AT during locomotion were calculated by fitting a quadratic function to the experimentally measured tendon force–length curve obtained from maximum voluntary isometric contractions. The maximum AT strain and force were affected by speed (p < 0.05, ranging from 4.0 to 4.9% strain and 1.989 to 2.556 kN), yet insufficient in magnitude to be considered as an effective stimulus for tendon adaptation. Besides the important tendon energy recoil during the propulsion phase (7.8 to 11.3 J), we found a recoil of elastic strain energy at the beginning of the stance phase of running (70–77 ms after touch down) between 1.7 ± 0.6 and 1.9 ± 1.1 J, which might be functionally relevant for running efficiency.
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Grange, Sylvain, Gustaaf Reurink, Anh Quoc Nguyen, Camille Riviera-Navarro, Clément Foschia, Pierre Croisille, and Pascal Edouard. "Location of Hamstring Injuries Based on Magnetic Resonance Imaging: A Systematic Review." Sports Health: A Multidisciplinary Approach, February 11, 2022, 194173812110710. http://dx.doi.org/10.1177/19417381211071010.
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Context: Hamstring muscle injury location using magnetic resonance imaging (MRI) is not so well described in the literature. Objective: To describe the location of hamstring injuries using MRI. Data Sources: PubMed, Web of Science, Scopus, SPORTDiscus, Cochrane Library. Study Selection: The full text of studies, in English, had to be available. Case reports and reviews were excluded. Included studies must report the location of hamstring injuries using MRI within 8 days of the acute injury. Study Design: Systematic review. Level of Evidence: Level 4. Data Extraction: A first screening was conducted based on title and abstract of the articles. In the second screening, the full text of the remaining articles was evaluated for the fulfillment of the inclusion criteria. Results: From the 2788 references initially found in 5 databases, we included 34 studies, reporting a total of 2761 acute hamstring injuries. The most frequent muscle head involved was the long head of the biceps femoris (BFLH) (70%), followed by the semitendinosus (ST) (15%), generally associated with BFLH. The most frequent tissue affected was the myotendinous junction (MTJ) accounting for half the cases (52%). Among all lesions, the distribution between proximal, central, and distal lesions looked homogenous, with 34.0%, 33.4% and 32.6%, respectively. The stretching mechanism, while only reported in 2 articles, represented 3% of all reported mechanisms, appears responsible for a specific lesion involving the proximal tendon of the semimembranosus (SM), and leading to a longer time out from sport. Conclusion: BFLH was the most often affected hamstring injuries and MTJ was the most affected tissue. In addition, the distal, central, and proximal locations were homogeneously distributed. We also noted that MRI descriptions of hamstring injuries are often poor and did not take full advantage of the MRI strengths. Systematic Review Registration: Before study initiation, the study was registered in the PROSPERO International prospective register of systematic reviews (registration number CRD42018107580).
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Gamble, Lauri-Jo, Debra A. Canapp, and Sherman O. Canapp. "Evaluation of Achilles Tendon Injuries with Findings from Diagnostic Musculoskeletal Ultrasound in Canines – 43 Cases." Veterinary Evidence 2, no. 3 (September 12, 2017). http://dx.doi.org/10.18849/ve.v2i3.92.
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<p><strong>Objective: </strong>The objective was to describe clinical and ultrasonographic characteristics of canine Achilles tendon injuries.</p><p><strong>Background:</strong> Even though there have been publications describing characteristics of the normal and injured Achilles tendon by diagnostic ultrasound, there has been no previous in-depth ultrasonic evaluation and characterisation of Achilles tendon strains.</p><p><strong>Evidentiary value:</strong> This is a retrospective case series report of 43 dogs that underwent musculoskeletal diagnostic ultrasound evaluation of their strained Achilles tendons, with and without surgical repair.</p><p><strong>Methods: </strong>Data was collected from medical records of patients from August 2009 to May 2016. Inclusion criteria for dogs included a diagnosis of Achilles tendon injury based on the presence of fibre pattern modification within one or more components of the Achilles mechanism on initial diagnostic ultrasound.</p><p><strong>Results:</strong> It was found on the diagnostic ultrasound that Achilles tendon injuries were strictly unilateral in 51.2% (n=22/43) of cases and bilateral on presentation in 48.8% (n=21/43) of cases. 18.2% of the unilateral case progressively became bilateral over time (n=4/22). The injury was partial in 90.7% (n=39/43) of the cases and all three components of the Achilles mechanism were completely disrupted in only 9.3% of the cases (n=4/43). The partial injuries incorporated changes within the fibre patterns of all 3 components of the Achilles in 53.8% (n=21/39) of the cases and alteration of both the gastrocnemius tendon (GT) and common tendon (CT) in 41.0% (n=16/39) of the cases. Grade III strains were predominant (44.3%), followed by grade I (28.6%) and grade II (27.1%). Damage occurred most commonly at the tendino-osseous insertion (77%), with injury occurring less frequently diffusely along the body of the tendon (12.5%) or at the musculotendinous junction (10.5%).</p><p><strong>Conclusion: </strong>Diagnostic musculoskeletal ultrasound was used to identify lesions of Achilles tendon consistent with different grade of strain, as well as identifying the specific region of injury. Diagnostic ultrasound findings were correlated to the surgical findings and previous literature.</p><p><strong>Application:</strong> Diagnostic musculoskeletal ultrasound provides a non-invasive diagnostic modality for patients suspected of having Achilles tendon strain. Further investigation is needed to establish treatment protocols based on ultrasonographic 3-tier grading scheme for Achilles tendon strain injury.</p><p><strong>Abbreviations: </strong>Common tendon (CT), computed tomography scan (CT scan), gastrocnemius tendon (GT), magnetic resonance imaging (MRI), myotendinous junction (MTJ), superficial digital flexor tendon (SDFT).</p><br /> <img src="https://www.veterinaryevidence.org/rcvskmod/icons/oa-icon.jpg" alt="Open Access" /> <img src="https://www.veterinaryevidence.org/rcvskmod/icons/pr-icon.jpg" alt="Peer Reviewed" />
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Welcker, Daniela, Cornelia Stein, Natalia Martins Feitosa, Joy Armistead, Jin-Li Zhang, Steffen Lütke, Andre Kleinridders, et al. "Hemicentin-1 is an essential extracellular matrix component of the dermal–epidermal and myotendinous junctions." Scientific Reports 11, no. 1 (September 9, 2021). http://dx.doi.org/10.1038/s41598-021-96824-4.
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AbstractThe extracellular matrix architecture is composed of supramolecular fibrillar networks that define tissue specific cellular microenvironments. Hemicentins (Hmcn1 and Hmcn2) are ancient and very large members (> 600 kDa) of the fibulin family, whose short members are known to guide proper morphology and functional behavior of specialized cell types predominantly in elastic tissues. However, the tissue distribution and function of Hemicentins within the cellular microenvironment of connective tissues has remained largely unknown. Performing in situ hybridization and immunofluorescence analyses, we found that mouse Hmcn1 and Hmcn2 show a complementary distribution throughout different tissues and developmental stages. In postnatal dermal–epidermal junctions (DEJ) and myotendinous junctions (MTJ), Hmcn1 is primarily produced by mesenchymal cells (fibroblasts, tenocytes), Hmcn2 by cells of epithelial origin (keratinocytes, myocytes). Hmcn1−/− mice are viable and show no overt phenotypes in tissue tensile strength and locomotion tests. However, transmission electron microscopy revealed ultrastructural basement membrane (BM) alterations at the DEJ and MTJ of Hmcn1−/− mice, pointing to a thus far unknown role of Hmcn1 for BM and connective tissue boundary integrity.