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Photobiomodulation and different macrophages phenotypes during muscle tissue repair

Souza NHC, Mesquita-Ferrari RA, Rodrigues MFSD, da Silva DFT, Ribeiro BG, Alves AN, Garcia MP, Nunes FD, da Silva Junior EM, França CM, Bussadori SK, Fernandes KPS

Journal of cellular and molecular medicine · 53 citas

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Cómo se estudió

Diseño
Estudio en animales (clasificado por nuestro filtro de IA)
Estudiado en
Animales
Resultado principal
Solo mecanismos

Quién lo pagó

Financiación
Financiación independiente
Gobierno
Fundação de Amparo à Pesquisa do Estado de São Paulo
Subvenciones
Fundação de Amparo à Pesquisa do Estado de São Paulo (13/07502-1)

Según 1 financiador declarado y la declaración de financiación del texto completo.

Publicación

Publicado
2018-07-19 · J Cell Mol Med · vol. 22 · número 10 · págs. 4922–4934
Editorial
Wiley
Citado
83 citas · más que el 92% de estudios similares · 3.1× el promedio de su campo
Impacto
Entre el 10 % más citado de su campo
Referencias
39 trabajos
Acceso
Acceso abierto (revista) · CC-BY
Áreas de investigación
Laser Applications in Dentistry and Medicine · Medical and Biological Ozone Research
Palabras clave
Phenotype, Tissue repair, Muscle tissue, Cell biology, Biology, Pathology, Medicine, Anatomy, Genetics, Gene
MeSH
muscles, muscle, skeletal, macrophages, animals, humans, rats, receptors, cell surface, antigens, cd, antigens, differentiation, myelomonocytic, regeneration, wound healing, cell differentiation, muscle development, low-level light therapy, cd163 antigen

12 autores

  • Nadhia Helena Costa Souza🇧🇷Universidade Nove de Julho
  • Raquel Agnelli Mesquita‐Ferrari🇧🇷Universidade Nove de Julho
  • Maria Fernanda Setúbal Destro Rodrigues🇧🇷Universidade Nove de Julho
  • Daniela de Fátima Teixeira da Silva🇧🇷Universidade Nove de Julho
  • Beatriz Guimarães Ribeiro🇧🇷Universidade Nove de Julho
  • Agnelo Neves Alves🇧🇷Universidade Nove de Julho
  • Mónica Pereira Garcia🇧🇷Universidade Nove de Julho
  • Fábio Daumas Nunes🇧🇷Universidade de São Paulo
  • Evaldo M. da Silva🇧🇷Universidade Nove de Julho
  • Cristiane Miranda França🇧🇷Universidade Nove de Julho
  • Sandra Kalil Bussadori🇧🇷Universidade Nove de Julho
  • Kristianne Porta Santos Fernandes🇧🇷 · autor de correspondenciaUniversidade Nove de Julho

Resumen

El texto original del estudio, en el idioma en que se publicó.

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.

Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial (CC BY).

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