Coordinated Induction of the Ubiquitin Conjugation Pathway Accompanies the Developmentally Programmed Death of Insect Skeletal Muscle

AbstractImmune cells are involved in skeletal muscle regeneration. The mechanism by which Treg cells are involved in the regeneration of injured skeletal muscle is still unclear. The purpose of this study was to explore the role of programmed death-1 in contused skeletal muscle regeneration, and to clarify the regulation of programmed death-1 on Treg cell generation and macrophage polarization, in order to deepen our understanding of the relationship between the immune system and injured skeletal muscle regeneration. The results show that programmed death-1 knockdown reduced the number of Treg cells and impaired contused skeletal muscle regeneration compared with those of wild-type mice. The number of pro-inflammatory macrophages in the contused skeletal muscle of programmed death-1 knockout mice increased, and the expression of pro-inflammatory factors and oxidative stress factors increased, while the number of anti-inflammatory macrophages and the expression of anti-inflammatory factors, antioxidant stress factors, and muscle regeneration-related factors decreased. These results suggest that programmed death-1 can promote contused skeletal muscle regeneration by regulating Treg cell generation and macrophage polarization.

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Induction of T-Cell Infiltration and Programmed Death Ligand 2 Expression by Adeno-Associated Virus in Rhesus Macaque Skeletal Muscle and Modulation by Prednisone

Human Gene Therapy ◽

10.1089/hum.2016.113 ◽

2017 ◽

Vol 28 (6) ◽

pp. 493-509 ◽

Cited By ~ 8

Author(s):

Megan L. Cramer ◽

Guohong Shao ◽

Louise R. Rodino-Klapac ◽

Louis G. Chicoine ◽

Paul T. Martin

Keyword(s):

Skeletal Muscle ◽

T Cell ◽

Rhesus Macaque ◽

Cell Infiltration ◽

Adeno Associated Virus ◽

T Cell Infiltration ◽

Programmed Death

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Anion-induced potentiation of contraction in insect skeletal muscle

Comparative Biochemistry and Physiology ◽

10.1016/0010-406x(69)91333-4 ◽

1969 ◽

Vol 28 (1) ◽

pp. 185-192 ◽

Cited By ~ 3

Author(s):

H. Huddart

Keyword(s):

Skeletal Muscle ◽

Insect Skeletal Muscle

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Hydrogen peroxide stimulates ubiquitin-conjugating activity and expression of genes for specific E2 and E3 proteins in skeletal muscle myotubes

AJP Cell Physiology ◽

10.1152/ajpcell.00129.2003 ◽

2003 ◽

Vol 285 (4) ◽

pp. C806-C812 ◽

Cited By ~ 226

Author(s):

Yi-Ping Li ◽

Yuling Chen ◽

Andrew S. Li ◽

Michael B. Reid

Keyword(s):

Skeletal Muscle ◽

Actinomycin D ◽

Underlying Mechanism ◽

Muscle Proteins ◽

Conjugation System ◽

Cell Extracts ◽

Expression Of Genes ◽

Ubiquitin Conjugation ◽

Muscle Catabolism ◽

Stimulation Of

Reactive oxygen species (ROS) are thought to promote muscle atrophy in chronic wasting diseases, but the underlying mechanism has not been determined. Here we show that H2O2 stimulates ubiquitin conjugation to muscle proteins through transcriptional regulation of the enzymes (E2 and E3 proteins) that conjugate ubiquitin to muscle proteins. Incubation of C2C12 myotubes with 100 μM H2O2 increased the rate of 125I-labeled ubiquitin conjugation to muscle proteins in whole cell extracts. This response required at least 4-h exposure to H2O2 and persisted for at least 24 h. Preincubating myotubes with cycloheximide or actinomycin D blocked H2O2 stimulation of ubiquitin-conjugating activity, suggesting that gene transcription is required. Northern blot analyses revealed that H2O2 upregulates expression of specific E3 and E2 proteins that are thought to regulate muscle catabolism, including atrogin1/MAFbx, MuRF1, and E214k. These results suggest that ROS stimulate protein catabolism in skeletal muscle by upregulating the ubiquitin conjugation system.

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