Molecular feature of neutrophils in immune microenvironment of muscle atrophy

You, Zongqi; Huang, Xinying; Xiang, Yaoxian; Dai, Junxi; Jiang, Junjian; Xu, Jian‐Guang

doi:10.1111/jcmm.17495

Cited by 7 publications

(3 citation statements)

References 97 publications

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“…Neutrophils are the first line of defense of the immune system against fungal and bacterial infections under physiological conditions. The diversity of their individual activities and participation in BPs (such as NETs) play a critical role in inflammatory responses, overall immune coordination, and disease development [19]. Many studies have shown that neutrophils and their migration and infiltration may lead to major signaling events in skeletal muscle atrophy; however, neutrophil invasion into muscles is still controversial to some extent [20,21].…”

Section: Discussionmentioning

confidence: 99%

Bioinformatics analysis of paravertebral muscles atrophy in adult degenerative scoliosis

Rong

Zhong

Zhang

et al. 2023

Preprint

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Paravertebral muscles (PVM) act as one of the major dynamic factors to maintain human upright activities and play a remarkable role in maintaining the balance of the trunk. Adult degenerative scoliosis (ADS) has become one of the important causes of disability in the elderly population owing to the changes in spinal biomechanics, atrophy and degeneration of PVM, and imbalance of the spine. Previously, many studies focused on the physical evaluation of PVM degeneration. However, the molecular biological changes are still not completely known. In this study, we established a rat model of scoliosis and performed the proteomic analysis of the PVM of ADS. The results showed that the degree of atrophy, muscle fat deposition, and fibrosis of the PVM of rats positively correlated with the angle of scoliosis. The proteomic results showed that 177 differentially expressed proteins were present in the ADS group, which included 105 upregulated proteins and 72 downregulated proteins compared with the PVM in individuals without spinal deformities. Through the construction of a protein–protein interaction network, 18 core differentially expressed proteins were obtained, which included fibrinogen beta chain, apolipoprotein E, fibrinogen gamma chain, thrombospondin-1, integrin alpha-6, fibronectin-1, platelet factor 4, coagulation factor XIII A chain, ras-related protein Rap-1b, platelet endothelial cell adhesion molecule 1, complement C1q subcomponent subunit A, cathepsin G, myeloperoxidase, von Willebrand factor, integrin beta-1, integrin alpha-1, leukocyte surface antigen CD47, and complement C1q subcomponent subunit B. Further analysis of the Kyoto Encyclopedia of Genes and Genomes pathway (KEGG) and immunofluorescence showed that the neutrophil extracellular traps (NETs) formation signaling pathway plays a major role in the pathogenesis of PVM degeneration in ADS. The results of the present study preliminarily laid the molecular biological foundation of PVM atrophy in ADS, which will provide a new therapeutic target for alleviating PVM atrophy and decreasing the occurrence of scoliosis.

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Section: Discussionmentioning

confidence: 99%

Bioinformatics analysis of paravertebral muscles atrophy in adult degenerative scoliosis

Rong

Zhong

Zhang

et al. 2023

Preprint

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“…Spaceflight is known to induce immune dysregulation 60,61 and the immune system also plays a role in mediating the skeletal muscle response to disuse and recovery. [62][63][64][65] The baseline immune dysfunction in A/J mice could have been exacerbated by SM and led to the particularly sensitive response of A/J to SM. This finding suggests that immune dysfunction experienced during spaceflight could increase the magnitude of skeletal muscle loss and that enhancing the strength of the immune system could attenuate skeletal muscle loss during spaceflight, though further investigation is needed to confirm this link.…”

Section: Discussionmentioning

confidence: 99%

Genetic Diversity Modulates The Physical And Transcriptomic Response Of Skeletal Muscle To Simulated Microgravity

Zeineddine

Friedman

Buettmann

et al. 2023

Preprint

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Developments in long-term space exploration necessitate advancements in countermeasures against microgravity-induced skeletal muscle loss. Astronaut data shows considerable variation in muscle loss in response to microgravity. Previous experiments suggest that genetic background influences the skeletal muscle response to unloading, but no in-depth analysis of genetic expression was performed. Here, we placed eight inbred founder strains of the diversity outbred mice (129S1/SvImJ, A/J, C57BL/6J, CAST/EiJ, NOD/ShiLtJ, NZO/HILtJ, PWK/PhJ, and WSB/EiJ) in simulated microgravity (SM) via hindlimb unloading for three weeks. Body weight, muscle morphology, muscle strength, protein synthesis marker expression, and RNA expression were collected. A/J and CAST/EiJ mice were most susceptible to SM-induced muscle loss, whereas NOD/ShiLtJ mice were the most protected. In response to SM, A/J and CAST/EiJ mice experienced reductions in body weight, muscle mass, muscle volume, and muscle cross-sectional area. A/J mice had the highest number of differentially expressed genes (68) and associated gene ontologies (328). Downregulation of immunological gene ontologies and genes encoding anabolic immune factors suggest that immune dysregulation contributes to the response of A/J mice to SM. Several muscle properties showed significant interactions between SM and mouse strain and a high degree of heritability. These data imply that genetic background plays a role in the degree of muscle loss in SM and that more individualized programs should be developed for astronauts to protect their skeletal muscles against microgravity on long term missions.

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“…Muscle-localized neutrophils are considered to release inflammatory cytokine, proteases, and free radicals, leading to exacerbated muscle atrophy ( 18 , 19 ). Furthermore, we found NETs were prominent in muscle on neutrophil-peaked day 14, suggesting that NETs may be associated with muscle atrophy and weakness.…”

Section: Discussionmentioning

confidence: 99%

Sepsis causes neutrophil infiltration in muscle leading to muscle atrophy and weakness in mice

Nakanishi¹,

Ono²,

Miyazaki³

et al. 2022

Front. Immunol.

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BackgroundSepsis-induced muscle atrophy leads to prolonged physical dysfunction. Although the interaction of muscle atrophy and macrophage has been reported in sepsis, the role of neutrophils in muscle atrophy has not been thoroughly investigated. This study sought to investigate the long-term changes in muscle-localized neutrophils after sepsis induction and their possible role in sepsis.MethodsSepsis was induced in seven-week-old male C57BL/6J mice 8-12 (cecal slurry [CS] model) via intraperitoneal injection of 1 mg/g cecal slurry. The percentage change in body weight and grip strength was evaluated. The tibialis anterior muscles were dissected for microscopic examination of the cross-sectional area of myofibers or Fluorescence-activated cell sorting (FACS) analysis of immune cells. These changes were evaluated in the following conditions: (1) Longitudinal change until day 61, (2) CS concentration-dependent change on day 14 at the low (0.3 mg/g), middle (1.0 mg/g), and high (2.0 mg/g) concentrations, and (3) CS mice on day 14 treated with an anti-Ly6G antibody that depletes neutrophils.ResultsBody weight and grip strength were significantly lower in the CS model until day 61 (body weight: 123.1% ± 1.8% vs. 130.3% ± 2.5%, p = 0.04; grip strength: 104.5% ± 3.8% vs. 119.3% ± 5.3%, p = 0.04). Likewise, cross-sectional muscle area gradually decreased until day 61 from the CS induction (895.6 [606.0–1304.9] μm2 vs. 718.8 [536.2–937.0] μm2, p < 0.01). The number of muscle-localized neutrophils increased from 2.3 ± 0.6 cell/mg on day 0 to 22.2 ± 13.0 cell/mg on day 14, and decreased thereafter. In terms of CS concentration–dependent change, cross-sectional area was smaller (484.4 ± 221.2 vs. 825.8 ± 436.2 μm2 [p < 0.001]) and grip strength was lower (71.4% ± 12.8% vs. 116.3% ± 7.4%, p = 0.01) in the CS High group compared with the control, with increased neutrophils (p = 0.03). Ly6G-depleted mice demonstrated significant increase of muscle cross-sectional area and grip strength compared with control mice (p < 0.01).ConclusionsSepsis causes infiltration of neutrophils in muscles, leading to muscle atrophy and weakness. Depletion of neutrophils in muscle reverses sepsis-induced muscle atrophy and weakness. These results suggest that neutrophils may play a critical role in sepsis-induced muscle atrophy and weakness.

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Molecular feature of neutrophils in immune microenvironment of muscle atrophy

Cited by 7 publications

References 97 publications

Bioinformatics analysis of paravertebral muscles atrophy in adult degenerative scoliosis

Bioinformatics analysis of paravertebral muscles atrophy in adult degenerative scoliosis

Genetic Diversity Modulates The Physical And Transcriptomic Response Of Skeletal Muscle To Simulated Microgravity

Sepsis causes neutrophil infiltration in muscle leading to muscle atrophy and weakness in mice

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