Structural and functional changes in the microvasculature of disused skeletal muscle

Tyml, Karel

doi:10.2741/a592

Cited by 36 publications

(29 citation statements)

References 35 publications

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“…ANG is also a potent stimulator of angiogenesis, specifically up-regulating the production of proteases that degrade laminin and fibronectin, allowing endothelial cells to migrate and form new vessels (45,46). This information suggests that lack of ANG production by pericytes during IM may contribute to suppression of protein synthesis and atrophy, as well as reductions to capillary number (C/F ratio) or capillary density (capillary per square millimeter tissue) following disuse (47)(48)(49)(50). In addition to the change in Ang gene expression, the increases in Atf4 and p53 in NG2 + Lin 2 pericytes post-IM were also striking.…”

Section: Discussionmentioning

confidence: 99%

Pericyte transplantation improves skeletal muscle recovery following hindlimb immobilization

et al. 2019

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Conditions of extended bed rest and limb immobilization can initiate rapid and significant loss of skeletal muscle mass and function. Physical rehabilitation is standard practice following a period of disuse, yet mobility may be severely compromised, and recovery is commonly delayed or incomplete in special populations. Thus, a novel approach toward recovery of muscle mass is highly desired. Pericytes [neuron‐glial antigen 2 (NG2)+CD31−CD45−(Lineage− [Lin−]) and CD146+Lin−] demonstrate capacity to facilitate muscle repair, yet the ability to enhance myofiber growth following disuse is unknown. In the current study, 3–4‐mo‐old mice were unilaterally immobilized for 14 d (IM) or immobilized for 14 d followed by 14 d of remobilization (RE). Flow cytometry and targeted gene expression analyses were completed to assess pericyte quantity and function following IM and RE. In addition, a transplantation study was conducted to assess the impact of pericytes on recovery. Results from targeted analyses suggest minimal impact of disuse on pericyte gene expression, yet NG2+Lin− pericyte quantity is reduced following IM (P < 0.05). Remarkably, pericyte transplantation recovered losses in myofiber cross‐sectional area and the capillary‐to‐fiber ratio following RE, whereas deficits remained with vehicle alone (P = 0.01). These findings provide the first evidence that pericytes effectively rehabilitate skeletal muscle mass following disuse atrophy.—Munroe, M., Dvoretskiy, S., Lopez, A., Leong, J., Dyle, M. C., Kong, H., Adams, C. M., Boppart, M. D. Pericyte transplantation improves skeletal muscle recovery following hindlimb immobilization. FASEB J. 33, 7694–7706 (2019). http://www.fasebj.org

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Section: Discussionmentioning

confidence: 99%

Pericyte transplantation improves skeletal muscle recovery following hindlimb immobilization

et al. 2019

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“…Although several studies explore acute skeletal muscle atrophy (eg, disuse, spaceflight, immobilization, or denervation [19,29,36,37], the molecular mechanisms of chronic atrophy after tendon tears are less well understood [11]. We presume an understanding of the cascade(s) of cellular processes that lead to muscle atrophy with tendon damage could lead to focused pharmacologic treatments (eg, proteolysis inhibitors) reversing the atrophy.…”

Section: Introductionmentioning

confidence: 97%

Expression of Atrophy mRNA Relates to Tendon Tear Size in Supraspinatus Muscle

Schmutz

Fuchs

Regenfelder

et al. 2009

Clinical Orthopaedics &Amp; Related Research

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Skeletal muscle atrophy and fatty infiltration develop after tendon tearing. The extent of atrophy serves as one prognostic factor for the outcome of surgical repair of rotator cuff tendon tears. We asked whether mRNA of genes involved in regulation of degradative processes leading to muscle atrophy, ie, FOXOs, MSTN, calpains, cathepsins, and transcripts of the ubiquitin-proteasome pathway, are overexpressed in the supraspinatus muscle in patients with and without rotator cuff tears. We evaluated biopsy specimens collected during surgery of 53 consecutive patients with different sizes of rotator cuff tendon tears and six without tears. The levels of corresponding gene transcripts in total RNA extracts were assessed by semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. Supraspinatus muscle atrophy was assessed by MRI. The area of muscle tissue (or atrophy), decreased (increased) with increasing tendon tear size. The transcripts of CAPN1, UBE2B, and UBE3A were upregulated more than twofold in massive rotator cuff tears as opposed to smaller tears or patients without tears. These atrophy gene products may be involved in cellular processes that impair functional recovery of affected muscles after surgical rotator cuff repair. However, the damaging effects of gene products in their respective proteolytic processes on muscle structures and proteins remains to be investigated.

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“…cytoarchitecture and composition; Chopard et al 2001;Frenette and Tidball 1998) and fibre-associated structures (i.e. nerves, capillaries; Tyml and Mathieu-Costello 2001;Deschenes et al 2001). Transcriptional reprogramming of nuclei is recognized to be a major event early on in this process (Wittwer et al 2002a;Carson et al 2002).…”

mentioning

confidence: 99%

Molecular basis of skeletal muscle plasticity-from gene to form and function

Flück

Hoppeler

2003

Reviews of Physiology, Biochemistry and Pharmacology

368

334

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Skeletal muscle shows an enormous plasticity to adapt to stimuli such as contractile activity (endurance exercise, electrical stimulation, denervation), loading conditions (resistance training, microgravity), substrate supply (nutritional interventions) or environmental factors (hypoxia). The presented data show that adaptive structural events occur in both muscle fibres (myofibrils, mitochondria) and associated structures (motoneurons and capillaries). Functional adaptations appear to involve alterations in regulatory mechanisms (neuronal, endocrine and intracellular signalling), contractile properties and metabolic capacities. With the appropriate molecular techniques it has been demonstrated over the past 10 years that rapid changes in skeletal muscle mRNA expression occur with exercise in human and rodent species. Recently, gene expression profiling analysis has demonstrated that transcriptional adaptations in skeletal muscle due to changes in loading involve a broad range of genes and that mRNA changes often run parallel for genes in the same functional categories. These changes can be matched to the structural/functional adaptations known to occur with corresponding stimuli. Several signalling pathways involving cytoplasmic protein kinases and nuclear-encoded transcription factors are recognized as potential master regulators that transduce physiological stress into transcriptional adaptations of batteries of metabolic and contractile genes. Nuclear reprogramming is recognized as an important event in muscle plasticity and may be related to the adaptations in the myosin type, protein turnover, and the cytoplasma-to-myonucleus ratio. The accessibility of muscle tissue to biopsies in conjunction with the advent of high-throughput gene expression analysis technology points to skeletal muscle plasticity as a particularly useful paradigm for studying gene regulatory phenomena in humans.Structure, function: bOX b-Oxidation · DEL Deltoidus · EC coupling Excitationcontraction coupling · EDL Extensor digitorum longus · Gls Glycolysis · H+ Reducing equivalents · IMF mitochondria Interfibrillar mitochondria · IMCL Intra-myocellular lipid · KC Krebs cycle · M Muscle · NMJ Neuromuscular junction · SR Sarcoplasmic reticulum · S mitochondria Subsarcolemmal mitochondria · Tn Troponin · VL Vastus lateralis · VO2max Maximal oxygen consumption Signals, sensors and transducers: ACTH Corticotropin · AMPK 5'-AMP-activated protein kinase · ATP Adenosine 5'-triphosphate · Ca2+ Intracellular calcium · CaMKII Ca 2+ /CaM kinase II · Cor Cortisol · EN Epinephrine · ERK Extracellular signal-regulated kinase · GH Growth hormone · IGFBP-3 Insulin-like growth factor binding protein 3 · IGF-I Insulin-like growth factor I · JNK c-jun N-terminal kinase · c-jun cellular counterpart of retroviral insert from avian sarcoma virus 17 · Ins Insulin · lep Leptin · MAPK Mitogen-activated (microtubule-associated) protein kinase · NRF-1 and -2 Nuclear respiratory factor 1 and 2 · p38 p38 MAPK · RE Renin · ROS Reactive oxygen species · T3 Triiodothyron...

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Structural and functional changes in the microvasculature of disused skeletal muscle

Cited by 36 publications

References 35 publications

Pericyte transplantation improves skeletal muscle recovery following hindlimb immobilization

Pericyte transplantation improves skeletal muscle recovery following hindlimb immobilization

Expression of Atrophy mRNA Relates to Tendon Tear Size in Supraspinatus Muscle

Molecular basis of skeletal muscle plasticity-from gene to form and function

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