Special Issue "Mechanobiology Defects in Muscular Disorders"

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (31 October 2020).

Special Issue Editor

Dr. Catherine Coirault
E-Mail Website
Guest Editor
Center of Research in Myology, Sorbonne University, INSERM 974, 75654 Paris, France
Interests: mechanobiology; mechanotransduction; nuclear envelope; muscular disorders
Special Issues and Collections in MDPI journals

Special Issue Information

Dear Colleagues,

Whereas the primary function of muscle is to produce force and movement, a vast body of research has accumulated to illustrate that mechanical forces in turn are critical to controlling muscle cell decisions and tissue homeostasis. It is becoming evident that mechanobiology defects are present in a wide range of muscular disorders, either inherited—such as muscular dystrophy—or acquired—such as age-related muscular diseases. The process of mechanobiology may be altered by changes in the extracellular matrix composition and stiffness, changes in muscle mechanics, or by the deregulation of the molecular mechanisms by which muscle cells and tissues sense and transduce mechanical force into biochemical signals. In a desire to develop new targets for therapeutic interventions, understanding the mechanical cues that regulate muscle development and homeostasis has become an active and fruitful area of research.

This Special Issue aims to provide comprehensible knowledge of mechanobiology defects in muscular disorders, including cell biology, molecular biology, and mechanobiology tools used in the muscle field. We invite the community to submit original articles or reviews in the above-mentioned field.

We look forward to your contributions

Dr. Catherine Coirault
Guest Editor

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2000 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • mechanical stress
  • mechanotransduction
  • mechanosensation
  • mechanoresponse
  • striated muscle
  • muscle homeostasis
  • muscle growth
  • myopathy

Published Papers (2 papers)

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Open AccessArticle
Perlecan Facilitates Neuronal Nitric Oxide Synthase Delocalization in Denervation-Induced Muscle Atrophy
Cells 2020, 9(11), 2524; https://doi.org/10.3390/cells9112524 - 23 Nov 2020
Cited by 1 | Viewed by 587
Abstract
Perlecan is an extracellular matrix molecule anchored to the sarcolemma by a dystrophin–glycoprotein complex. Perlecan-deficient mice are tolerant to muscle atrophy, suggesting that perlecan negatively regulates mechanical stress-dependent skeletal muscle mass. Delocalization of neuronal nitric oxide synthase (nNOS) from the sarcolemma to the [...] Read more.
Perlecan is an extracellular matrix molecule anchored to the sarcolemma by a dystrophin–glycoprotein complex. Perlecan-deficient mice are tolerant to muscle atrophy, suggesting that perlecan negatively regulates mechanical stress-dependent skeletal muscle mass. Delocalization of neuronal nitric oxide synthase (nNOS) from the sarcolemma to the cytosol triggers protein degradation, thereby initiating skeletal muscle atrophy. We hypothesized that perlecan regulates nNOS delocalization and activates protein degradation during this process. To determine the role of perlecan in nNOS-mediated mechanotransduction, we used sciatic nerve transection as a denervation model of gastrocnemius muscles. Gastrocnemius muscle atrophy was significantly lower in perinatal lethality-rescued perlecan-knockout (Hspg2−/−-Tg) mice than controls (WT-Tg) on days 4 and 14 following surgery. Immunofluorescence microscopy showed that cell membrane nNOS expression was reduced by denervation in WT-Tg mice, with marginal effects in Hspg2−/−-Tg mice. Moreover, levels of atrophy-related proteins—i.e., FoxO1a, FoxO3a, atrogin-1, and Lys48-polyubiquitinated proteins—increased in the denervated muscles of WT-Tg mice but not in Hspg2−/−-Tg mice. These findings suggest that during denervation, perlecan promotes nNOS delocalization from the membrane and stimulates protein degradation and muscle atrophy by activating FoxO signaling and the ubiquitin–proteasome system. Full article
(This article belongs to the Special Issue Mechanobiology Defects in Muscular Disorders)
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Review

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Open AccessReview
Nuclear Mechanotransduction in Skeletal Muscle
Cells 2021, 10(2), 318; https://doi.org/10.3390/cells10020318 - 04 Feb 2021
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Abstract
Skeletal muscle is composed of multinucleated, mature muscle cells (myofibers) responsible for contraction, and a resident pool of mononucleated muscle cell precursors (MCPs), that are maintained in a quiescent state in homeostatic conditions. Skeletal muscle is remarkable in its ability to adapt to [...] Read more.
Skeletal muscle is composed of multinucleated, mature muscle cells (myofibers) responsible for contraction, and a resident pool of mononucleated muscle cell precursors (MCPs), that are maintained in a quiescent state in homeostatic conditions. Skeletal muscle is remarkable in its ability to adapt to mechanical constraints, a property referred as muscle plasticity and mediated by both MCPs and myofibers. An emerging body of literature supports the notion that muscle plasticity is critically dependent upon nuclear mechanotransduction, which is transduction of exterior physical forces into the nucleus to generate a biological response. Mechanical loading induces nuclear deformation, changes in the nuclear lamina organization, chromatin condensation state, and cell signaling, which ultimately impacts myogenic cell fate decisions. This review summarizes contemporary insights into the mechanisms underlying nuclear force transmission in MCPs and myofibers. We discuss how the cytoskeleton and nuclear reorganizations during myogenic differentiation may affect force transmission and nuclear mechanotransduction. We also discuss how to apply these findings in the context of muscular disorders. Finally, we highlight current gaps in knowledge and opportunities for further research in the field. Full article
(This article belongs to the Special Issue Mechanobiology Defects in Muscular Disorders)
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