Interleukin-6/Signal Transducer and Activator of Transcription 3 (STAT3) Pathway Is Essential for Macrophage Infiltration and Myoblast Proliferation during Muscle Regeneration

Zhang, Congcong; Li, Yulin; Wu, Yina; Wang, Luya; Wang, Xiaonan; Du, Jie

doi:10.1074/jbc.m112.419788

Cited by 246 publications

(221 citation statements)

References 37 publications

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“…27 IL-6 knockout mice were shown to have an impaired hypertrophic response to overloading. 28 We previously reported that myogenesis response to muscle injury was blunted in IL-6 knockout mice, 29 which proved the positive effect of IL-6 on myogenesis. Other groups have also reported that electrical stimulation increases IL-6 in both cultured C2C12 cells 30 and human primary muscle cells.…”

Section: Discussionmentioning

confidence: 85%

Low-Frequency Electrical Stimulation Attenuates Muscle Atrophy in CKD—A Potential Treatment Strategy

Klein

Hassounah

et al. 2015

Journal of the American Society of Nephrology

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Effective therapeutic strategies to treat CKD-induced muscle atrophy are urgently needed. Lowfrequency electrical stimulation (LFES) may be effective in preventing muscle atrophy, because LFES is an acupuncture technique that mimics resistance exercise by inducing muscle contraction. To test this hypothesis, we treated 5/6-nephrectomized mice (CKD mice) and control mice with LFES for 15 days. LFES prevented soleus and extensor digitorum longus muscle weight loss and loss of hind-limb muscle grip in CKD mice. LFES countered the CKD-induced decline in the IGF-1 signaling pathway and led to increases in markers of protein synthesis and myogenesis and improvement in muscle protein metabolism. In control mice, we observed an acute response phase immediately after LFES, during which the expression of inflammatory cytokines (IFN-g and IL-6) increased. Expression of the M1 macrophage marker IL-1b also increased acutely, but expression of the M2 marker arginase-1 increased 2 days after initiation of LFES, paralleling the change in IGF-1. In muscle cross-sections of LFES-treated mice, arginase-1 colocalized with IGF-1. Additionally, expression of microRNA-1 and -206, which inhibits IGF-1 translation, decreased in the acute response phase after LFES and increased at a later phase. We conclude that LFES ameliorates CKDinduced skeletal muscle atrophy by upregulation of the IGF-1 signaling pathway, which improves protein metabolism and promotes myogenesis. The upregulation of IGF-1 may be mediated by decreased expression of microRNA-1 and -206 and/or activation of M2 macrophages.

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Section: Discussionmentioning

confidence: 85%

Low-Frequency Electrical Stimulation Attenuates Muscle Atrophy in CKD—A Potential Treatment Strategy

Klein

Hassounah

et al. 2015

Journal of the American Society of Nephrology

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“…The effects of PBM on macrophage phenotypes are beginning to be described in cell cultures studies,10, 30, 31, 32, 33, 34 evidencing that this therapeutic modality, especially using the NIR wavelength, is capable of altering the polarization of these cells in vitro. In vivo experiments have demonstrated that PBM (808 nm) can shift the phenotype of brain microglial polarization from the pro‐inflammatory phenotype (M1) to the anti‐inflammatory (M2) phenotype after ischemic stroke, promoting cortical neurogenesis 35.…”

Section: Discussionmentioning

confidence: 99%

Photobiomodulation and different macrophages phenotypes during muscle tissue repair

Souza

Mesquita‐Ferrari

Rodrigues

et al. 2018

J Cellular Molecular Medi

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Macrophages play a very important role in the conduction of several regenerative processes mainly due to their plasticity and multiple functions. In the muscle repair process, while M1 macrophages regulate the inflammatory and proliferative phases, M2 (anti‐inflammatory) macrophages direct the differentiation and remodelling phases, leading to tissue regeneration. The aim of this study was to evaluate the effect of red and near infrared (NIR) photobiomodulation (PBM) on macrophage phenotypes and correlate these findings with the repair process following acute muscle injury. Wistar rats were divided into 4 groups: control; muscle injury; muscle injury + red PBM; and muscle injury + NIR PBM. After 2, 4 and 7 days, the tibialis anterior muscle was processed for analysis. Macrophages phenotypic profile was evaluated by immunohistochemistry and correlated with the different stages of the skeletal muscle repair by the qualitative and quantitative morphological analysis as well as by the evaluation of IL‐6,TNF‐α and TGF‐β mRNA expression. Photobiomodulation at both wavelengths was able to decrease the number of CD68+ (M1) macrophages 2 days after muscle injury and increase the number of CD163+ (M2) macrophages 7 days after injury. However, only NIR treatment was able to increase the number of CD206+ M2 macrophages (Day 2) and TGF ‐β mRNA expression (Day 2, 4 and 7), favouring the repair process more expressivelly. Treatment with PBM was able to modulate the inflammation phase, optimize the transition from the inflammatory to the regeneration phase (mainly with NIR light) and improve the final step of regeneration, enhancing tissue repair.

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“…It is likely that macrophages and stromal cells bidirectionally communicate to support repair in several different tissue microenvironments. For instance, macrophages are necessary for the formation of niches required for limb regeneration in salamanders (74), for skeletal muscle regeneration following toxinmediated injury (75), and for cardiac regeneration in neonatal mice after MI (38). With a growing appreciation for macrophage heterogeneity, it will be important to delineate the factors governing the polarization (denoted by transcriptional regulation and expression of surface markers) of macrophages during ischemic injury (24,25,43).…”

Section: Macrophage Cell Isolation and Differentiationmentioning

confidence: 99%

Macrophages mediate cardioprotective cellular postconditioning in acute myocardial infarction

et al. 2015

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R e s e a R c h a R t i c l e 3 1 4 8jci.org Volume 125 Number 8 August 2015angioplasty to reopen the occluded coronary artery. After flow has been reestablished, the use of adjunctive therapy can be considered without distraction. Adjunctive cell therapy would require thawing of an allogeneic, off-the-shelf product and preparation for administration, which could introduce a delay of up to 20 minutes. Therefore, in our rat model, we subjected rats to 45 minutes of ischemia, followed by 20 minutes of reperfusion. Cells (or vehicle) were then delivered to the coronary circulation ( Figure 1A). To examine whether cell administration could by adoptive transfer of CDC-primed macrophages. Distinctive changes in macrophage gene expression and function underlie the cardioprotective effects of CDCs.

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Interleukin-6/Signal Transducer and Activator of Transcription 3 (STAT3) Pathway Is Essential for Macrophage Infiltration and Myoblast Proliferation during Muscle Regeneration

Cited by 246 publications

References 37 publications

Low-Frequency Electrical Stimulation Attenuates Muscle Atrophy in CKD—A Potential Treatment Strategy

Low-Frequency Electrical Stimulation Attenuates Muscle Atrophy in CKD—A Potential Treatment Strategy

Photobiomodulation and different macrophages phenotypes during muscle tissue repair

Macrophages mediate cardioprotective cellular postconditioning in acute myocardial infarction

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