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      Photobiomodulation and different macrophages phenotypes during muscle tissue repair

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          Abstract

          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 , TNFα and TGFβ 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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          Most cited references30

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          Understanding the Mysterious M2 Macrophage through Activation Markers and Effector Mechanisms

          The alternatively activated or M2 macrophages are immune cells with high phenotypic heterogeneity and are governing functions at the interface of immunity, tissue homeostasis, metabolism, and endocrine signaling. Today the M2 macrophages are identified based on the expression pattern of a set of M2 markers. These markers are transmembrane glycoproteins, scavenger receptors, enzymes, growth factors, hormones, cytokines, and cytokine receptors with diverse and often yet unexplored functions. This review discusses whether these M2 markers can be reliably used to identify M2 macrophages and define their functional subdivisions. Also, it provides an update on the novel signals of the tissue environment and the neuroendocrine system which shape the M2 activation. The possible evolutionary roots of the M2 macrophage functions are also discussed.
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            Regulatory interactions between muscle and the immune system during muscle regeneration.

            Recent discoveries reveal complex interactions between skeletal muscle and the immune system that regulate muscle regeneration. In this review, we evaluate evidence that indicates that the response of myeloid cells to muscle injury promotes muscle regeneration and growth. Acute perturbations of muscle activate a sequence of interactions between muscle and inflammatory cells. The initial inflammatory response is a characteristic Th1 inflammatory response, first dominated by neutrophils and subsequently by CD68(+) M1 macrophages. M1 macrophages can propagate the Th1 response by releasing proinflammatory cytokines and cause further tissue damage through the release of nitric oxide. Myeloid cells in the early Th1 response stimulate the proliferative phase of myogenesis through mechanisms mediated by TNF-alpha and IL-6; experimental prolongation of their presence is associated with delayed transition to the early differentiation stage of myogenesis. Subsequent invasion by CD163(+)/CD206(+) M2 macrophages attenuates M1 populations through the release of anti-inflammatory cytokines, including IL-10. M2 macrophages play a major role in promoting growth and regeneration; their absence greatly slows muscle growth following injury or modified use and inhibits muscle differentiation and regeneration. Chronic muscle injury leads to profiles of macrophage invasion and function that differ from acute injuries. For example, mdx muscular dystrophy yields invasion of muscle by M1 macrophages, but their early invasion is accompanied by a subpopulation of M2a macrophages. M2a macrophages are IL-4 receptor(+)/CD206(+) cells that reduce cytotoxicity of M1 macrophages. Subsequent invasion of dystrophic muscle by M2c macrophages is associated with progression of the regenerative phase in pathophysiology. Together, these findings show that transitions in macrophage phenotype are an essential component of muscle regeneration in vivo following acute or chronic muscle damage.
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              Interleukin‐6 myokine signaling in skeletal muscle: a double‐edged sword?

              Interleukin (IL)‐6 is a cytokine with pleiotropic functions in different tissues and organs. Skeletal muscle produces and releases significant levels of IL‐6 after prolonged exercise and is therefore considered as a myokine. Muscle is also an important target of the cytokine. IL‐6 signaling has been associated with stimulation of hypertrophic muscle growth and myogenesis through regulation of the proliferative capacity of muscle stem cells. Additional beneficial effects of IL‐6 include regulation of energy metabolism, which is related to the capacity of actively contracting muscle to synthesize and release IL‐6. Paradoxically, deleterious actions for IL‐6 have also been proposed, such as promotion of atrophy and muscle wasting. We review the current evidence for these apparently contradictory effects, the mechanisms involved and discuss their possible biological implications.
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                Author and article information

                Contributors
                kristianneporta@gmail.com
                Journal
                J Cell Mol Med
                J. Cell. Mol. Med
                10.1111/(ISSN)1582-4934
                JCMM
                Journal of Cellular and Molecular Medicine
                John Wiley and Sons Inc. (Hoboken )
                1582-1838
                1582-4934
                19 July 2018
                October 2018
                : 22
                : 10 ( doiID: 10.1111/jcmm.2018.22.issue-10 )
                : 4922-4934
                Affiliations
                [ 1 ] Postgraduate Program in Rehabilition Sciences Nove de Julho University (UNINOVE) São Paulo Brazil
                [ 2 ] Postgraduate Program in Biophotonics Applied to Health Sciences Nove de Julho University (UNINOVE) São Paulo Brazil
                [ 3 ] Departament of Oral Pathology School of Dentistry University of São Paulo (FOUSP) São Paulo Brazil
                Author notes
                [*] [* ] Correspondence

                Kristianne Porta Santos Fernandes

                Email: kristianneporta@ 123456gmail.com

                Author information
                http://orcid.org/0000-0001-5142-9526
                http://orcid.org/0000-0002-3067-9224
                http://orcid.org/0000-0002-7228-6146
                http://orcid.org/0000-0003-2586-4377
                http://orcid.org/0000-0002-7785-6785
                http://orcid.org/0000-0002-9853-1138
                http://orcid.org/0000-0001-7156-9286
                Article
                JCMM13757
                10.1111/jcmm.13757
                6156453
                30024093
                a593b77e-0425-4ea8-a374-c1a2185bcbfc
                © 2018 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 01 March 2018
                : 09 June 2018
                Page count
                Figures: 6, Tables: 1, Pages: 13, Words: 7197
                Funding
                Funded by: Fundação de Amparo à Pesquisa do Estado de São Paulo, São Paulo Research Foundation ‐ FAPESP
                Award ID: 2013/07502‐1
                Categories
                Original Article
                Original Articles
                Custom metadata
                2.0
                jcmm13757
                October 2018
                Converter:WILEY_ML3GV2_TO_NLMPMC version:version=5.4.9 mode:remove_FC converted:26.09.2018

                Molecular medicine
                macrophages,muscle,photobiomodulation,regeneration,regenerative medicine
                Molecular medicine
                macrophages, muscle, photobiomodulation, regeneration, regenerative medicine

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