Redox cross talk from motor nerves to skeletal muscle regulates muscle redox homeostasis

2021 ◽  
Vol 177 ◽  
pp. S60
Author(s):  
Malcolm J. Jackson ◽  
Natalie Pollock ◽  
Caroline Staunton ◽  
Kay Hemmings ◽  
Aphrodite Vasilaki ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cross Talk ◽  
Redox Homeostasis ◽  
Motor Nerves

IRAK-1/IRS-1 Signaling Cross Talk in Human Skeletal Muscle—Role in Insulin Resistance

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 159-OR
Author(s):  
THEODORE P. CIARALDI ◽  
SUNDER MUDALIAR ◽  
LIWU LI ◽  
ROSARIO SCALIA ◽  
XIAO JIAN SUN ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Cross Talk ◽  
Human Skeletal Muscle

scholarly journals Strigolactone GR24 upregulates Nrf2 target genes and may protect against oxidative stress in skeletal muscle

F1000Research ◽  
2018 ◽  
Vol 7 ◽  
pp. 1459
Author(s):  
Shalem Raju Modi ◽  
Tarja Kokkola
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Skeletal Muscle ◽  
Transcription Factor ◽  
Stress Responses ◽  
Mycorrhizal Fungi ◽  
Target Genes ◽  
Redox Homeostasis ◽  
Antioxidant Defences ◽  
Microarray Gene Expression

GR24 is a synthetic strigolactone analog, demonstrated to regulate the development of plants and arbuscular mycorrhizal fungi. GR24 possesses anti-cancer and anti-apoptotic properties, enhances insulin sensitivity and mitochondrial biogenesis in skeletal myotubes, inhibits adipogenesis, decreases inflammation in adipocytes and macrophages and downregulates the expression of hepatic gluconeogenic enzymes. Transcription factor Nrf2 (Nuclear factor (erythroid-derived 2)-like 2) is a master regulator of antioxidant response, regulating a multitude of genes involved in cellular stress responses and anti-inflammatory pathways, thus maintaining cellular redox homeostasis. Nrf2 activation reduces the deleterious effects of mitochondrial toxins and has multiple roles in promoting mitochondrial function and dynamics. We studied the role of GR24 on gene expression in rat L6 skeletal muscle cells which were differentiated into myotubes. The myotubes were treated with GR24 and analyzed by microarray gene expression profiling. GR24 upregulated the cytoprotective transcription factor Nrf2 and its target genes, activating antioxidant defences, suggesting that GR24 may protect skeletal muscle from the toxic effects of oxidative stress.

scholarly journals Post-exercise cold-water immersion increases Na+,K+-ATPase α2-isoform mRNA content in parallel with elevated Sp1 expression in human skeletal muscle

2017 ◽  
Author(s):  
Danny Christiansen ◽  
Robyn M. Murphy ◽  
James R. Broatch ◽  
Jens Bangsbo ◽  
Michael J. McKenna ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Human Skeletal Muscle ◽  
Cold Water ◽  
Water Immersion ◽  
Redox Homeostasis ◽  
Cold Water Immersion ◽  
Post Exercise ◽  
Interval Exercise ◽  
Mrna Content ◽  
Exercise Induced

AbstractWe investigated the effect of a session of sprint-interval exercise on the mRNA content of NKA isoforms (α1-3, β1-3) and FXYD1 in human skeletal muscle. To explore some of the cellular stressors involved in this regulation, we evaluated the association between these mRNA responses and those of the transcription factors Sp1, Sp3 and HIF-1α. Given cold exposure perturbs muscle redox homeostasis, which may be one mechanism important for increases in NKA-isoform mRNA, we also explored the effect of post-exercise cold-water immersion (CWI) on the mRNA responses. Muscle was sampled from nineteen men before (Pre) and after (+0h, +3h) exercise plus passive rest (CON, n=10) or CWI (10°C; COLD, n=9). In COLD, exercise increased NKAα2 and Sp1 mRNA (+0h, p<0.05). These genes remained unchanged in CON (p>0.05). In both conditions, exercise increased NKAα1, NKAβ3 and HIF-1α mRNA (+3h; p <0.05), decreased NKAβ2 mRNA (+3h; p<0.05), whereas NKAα3, NKAβ1, FXYD1 and Sp3 mRNA remained unchanged (p>0.05). These human findings highlight 1) sprint-interval exercise increases the mRNA content of NKA α1 and β3, and decreases that of NKA β2, which may relate, in part, to exercise-induced muscle hypoxia, and 2) post-exercise CWI augments NKAα2 mRNA, which may be associated with promoted Sp1 activation.

scholarly journals An in vitro injury model to examine pericyte‐skeletal muscle cell cross talk

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Katherine E LaBarbera ◽  
Kevin S O'Fallon ◽  
Priscilla M Clarkson ◽  
Sarah Witkowski
Keyword(s):  
Skeletal Muscle ◽  
Muscle Cell ◽  
Cross Talk ◽  
Skeletal Muscle Cell ◽  
Injury Model

scholarly journals Cross-Talk Between Extracellular Matrix and Skeletal Muscle: Implications for Myopathies

2020 ◽  
Vol 11 ◽  
Author(s):  
Khurshid Ahmad ◽  
Sibhghatulla Shaikh ◽  
Syed Sayeed Ahmad ◽  
Eun Ju Lee ◽  
Inho Choi
Keyword(s):  
Skeletal Muscle ◽  
Extracellular Matrix ◽  
Cross Talk

scholarly journals Exercise-Induced Mitohormesis for the Maintenance of Skeletal Muscle and Healthspan Extension

Sports ◽  
2019 ◽  
Vol 7 (7) ◽  
pp. 170 ◽  
Author(s):  
Robert V. Musci ◽  
Karyn L. Hamilton ◽  
Melissa A. Linden
Keyword(s):  
Skeletal Muscle ◽  
Oxidative Damage ◽  
Aerobic Exercise ◽  
Muscle Protein ◽  
Redox Homeostasis ◽  
Future Research ◽  
Skeletal Muscle Protein ◽  
Skeletal Muscle Function ◽  
Age Related ◽  
Nrf2 Signaling Pathway

Oxidative damage is one mechanism linking aging with chronic diseases including the progressive loss of skeletal muscle mass and function called sarcopenia. Thus, mitigating oxidative damage is a potential avenue to prevent or delay the onset of chronic disease and/or extend healthspan. Mitochondrial hormesis (mitohormesis) occurs when acute exposure to stress stimulates adaptive mitochondrial responses that improve mitochondrial function and resistance to stress. For example, an acute oxidative stress via mitochondrial superoxide production stimulates the activation of endogenous antioxidant gene transcription regulated by the redox sensitive transcription factor Nrf2, resulting in an adaptive hormetic response. In addition, acute stresses such as aerobic exercise stimulate the expansion of skeletal muscle mitochondria (i.e., mitochondrial biogenesis), constituting a mitohormetic response that protects from sarcopenia through a variety of mechanisms. This review summarized the effects of age-related declines in mitochondrial and redox homeostasis on skeletal muscle protein homeostasis and highlights the mitohormetic mechanisms by which aerobic exercise mitigates these age-related declines and maintains function. We discussed the potential efficacy of targeting the Nrf2 signaling pathway, which partially mediates adaptation to aerobic exercise, to restore mitochondrial and skeletal muscle function. Finally, we highlight knowledge gaps related to improving redox signaling and make recommendations for future research.

scholarly journals Proteome-wide Changes in the mdx-4cv Spleen due to Pathophysiological Cross Talk with Dystrophin-Deficient Skeletal Muscle

iScience ◽  
2020 ◽  
Vol 23 (9) ◽  
pp. 101500
Author(s):  
Paul Dowling ◽  
Stephen Gargan ◽  
Margit Zweyer ◽  
Michael Henry ◽  
Paula Meleady ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cross Talk
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