Unloading during skeletal muscle regeneration retards iNOS-expressing macrophage recruitment and perturbs satellite cell accumulation

Kawashima, Masato; Miyakawa, Motoi; Sugiyama, Megumi; Miyoshi, Makoto; Arakawa, Takamitsu

doi:10.1007/s00418-020-01897-3

Cited by 8 publications

(6 citation statements)

References 39 publications

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“…Additional immunostaining using iNOS, a representative M1 marker of macrophages (11,24), showed that the accumulation patterns of F4/80 þ iNOS þ cells (Fig. 3) were similar with those of F4/80 þ CD206 À cells at day 3 in the non-icing group (Fig.…”

Section: Phenotypic Dynamics Of Macrophages In the Damaged Musclementioning

confidence: 61%

“…Muscle regeneration was quantified by measuring the cross-sectional area (CSA) of centrally nucleated regenerating myofibers at day 14 after EC using the previously reported method (24,25). Briefly, at Â20 magnification of objective lens, five sections from each specimen separated by !50 μm underwent H&E staining, and five nonoverlapping areas of each section were digitally captured.…”

Section: Morphological Analysismentioning

confidence: 99%

“…Using double immunolabeling for F4/80 (a pan-macrophage marker) and CD206, M1 and M2 macrophages could be detected as F4/ 80 þ CD206 À and F4/80 þ CD206 þ cells, respectively, in the same section. The cell number quantification of these macrophages and Pax7 þ cells was performed as reported elsewhere (18,24). Briefly, at Â40 magnification of objective lens, 10 fields were captured per animal.…”

Section: Quantitative Analyses Of Macrophages and Pax7 þ Cellsmentioning

confidence: 99%

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Icing after eccentric contraction-induced muscle damage perturbs the disappearance of necrotic muscle fibers and phenotypic dynamics of macrophages in mice

Kawashima

Kawanishi

Tominaga

et al. 2021

Journal of Applied Physiology

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Icing is still one of the most common treatments to acute skeletal muscle damage in sports medicine. However, previous studies using rodents reported the detrimental effect of icing on muscle regeneration following injury. This study aimed to elucidate the critical factors governing the impairment of muscle regeneration by icing with a murine model of eccentric contraction-induced muscle damage by electrical stimulation. Because of icing after muscle injury, the infiltration of polynuclear and mononuclear cells into necrotic muscle fibers was retarded and attenuated, leading to the persistent presence of necrotic cellular debris. These phenomena coincided with the delayed emergence and sustained accumulation of Pax7+ myogenic cells within the regenerating area. Additionally, due to icing, delayed and/or sustained infiltration of M1 macrophages was noted in accordance with the perturbed expression patterns of inflammation-related factors, including tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10). The key myogenic regulatory factors (i.e., MyoD and myogenin) involved in the activation/proliferation and differentiation of myogenic precursor cells were not altered by icing during the regenerative process. A detailed analysis of regenerating myofibers by size distribution at day 14 after muscle damage showed that the ratio of small regenerating fibers to total regenerating fibers was higher in icing-treated animals than in untreated animals. These findings suggest that icing following muscle damage blunts the efficiency of muscle regeneration by perturbing the removal of necrotic myofibers and phenotypic dynamics of macrophages rather than affecting myogenic factors.

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Section: Phenotypic Dynamics Of Macrophages In the Damaged Musclementioning

confidence: 61%

Section: Morphological Analysismentioning

confidence: 99%

Section: Quantitative Analyses Of Macrophages and Pax7 þ Cellsmentioning

confidence: 99%

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Icing after eccentric contraction-induced muscle damage perturbs the disappearance of necrotic muscle fibers and phenotypic dynamics of macrophages in mice

Kawashima

Kawanishi

Tominaga

et al. 2021

Journal of Applied Physiology

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“…Therefore, the coordination of the inflammatory response and repair relationship after skeletal muscle injury is particularly important. NO can activate skeletal muscle myoblasts and participate in skeletal muscle regeneration in the process of acute and chronic injury of skeletal muscle (Qi et al, 2004;Zimiani et al, 2005;Wang et al, 2009;Kawashima et al, 2020). Exploring the molecular inflammation mechanism is conducive to understanding the mechanism by which NO alleviates skeletal muscle injury.…”

Section: Discussionmentioning

confidence: 99%

Effects of Nitric Oxide on C2C12 Cell Inflammatory Responses and Notexin-Induced Muscle Injury

et al. 2022

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Skeletal muscle injury is an acute inflammatory condition caused by an inflammatory response. To reduce inflammatory cell infiltration and relieve skeletal muscle injury, efficient treatment is urgently needed. Nitric oxide is a free radical molecule reported to have anti-inflammatory effects. In this study, we showed that NO could inhibit the inflammatory response of C2C12 cells in vitro and protect rat skeletal muscle injury from notexin in vivo. NO synthase inhibitor (L-NG-Nitroarginine Methyl Este, L-NAME) and NO donor (sodium nitroprusside dehydrate, SNP) were used to explore the vital role of lipopolysaccharides (LPSs) in LPS-stimulated C2C12 myoblasts.The expression of IL-18 and IL-1β was upregulated by L-NAME and downregulated by SNP, as indicated by the ELISA results. NO can reduce ASC, Caspase-1, and NLRP3 mRNA and protein levels. Furthermore, NO was detected in the rat model. The results of immunohistochemical staining showed that the production of DMD decreased. We conducted qRT-PCR and western blotting to detect the expression of Jo-1, Mi-2, TLR2, and TLR4 on day 6 post injury following treatment with L-NAME and SNP. The expression of Jo-1, Mi-2, TLR2, and TLR4 was upregulated by L-NAME and significantly reversed by SNP. NO can alleviate C2C12 cell inflammatory responses and protect rat skeletal muscle injury from notexin.

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“…Unloading has been shown to negatively influence muscle regeneration, since it retards the migration of macrophages into the injured site (Matsuba et al 2009;Kohno et al 2012). Now, Kawashima et al (2020) investigated the effect of hindlimb unloading as compared to weight-bearing control animals on the spatiotemporal behavior of iNOS-expressing macrophages (Fig. 1) and satellite cell accumulation after crush-induced muscle injury in rats.…”

Section: Unloading Impairs Muscle Regeneration: the Role Of Inos-expressing Macrophagesmentioning

confidence: 99%

In focus in HCB

Taatjes

Roth

2020

Histochem Cell Biol

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Unloading during skeletal muscle regeneration retards iNOS-expressing macrophage recruitment and perturbs satellite cell accumulation

Cited by 8 publications

References 39 publications

Icing after eccentric contraction-induced muscle damage perturbs the disappearance of necrotic muscle fibers and phenotypic dynamics of macrophages in mice

Icing after eccentric contraction-induced muscle damage perturbs the disappearance of necrotic muscle fibers and phenotypic dynamics of macrophages in mice

Effects of Nitric Oxide on C2C12 Cell Inflammatory Responses and Notexin-Induced Muscle Injury

In focus in HCB

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