Alterations in macrophage polarization in injured murine vocal folds.
Animals
Male
Mice
Cell Proliferation
Immunohistochemistry
Lectins, C-Type
/ metabolism
Macrophages
/ metabolism
Mannose Receptor
Mannose-Binding Lectins
/ metabolism
Mice, Inbred C57BL
Nitric Oxide Synthase Type II
/ metabolism
Phenotype
Random Allocation
Receptors, Cell Surface
/ metabolism
Vocal Cords
/ cytology
Wound Healing
Vocal fold
macrophage
polarization
Journal
The Laryngoscope
ISSN: 1531-4995
Titre abrégé: Laryngoscope
Pays: United States
ID NLM: 8607378
Informations de publication
Date de publication:
04 2019
04 2019
Historique:
accepted:
30
07
2018
pubmed:
1
1
2019
medline:
21
5
2019
entrez:
1
1
2019
Statut:
ppublish
Résumé
Macrophages are prominent inflammatory cells in wounds, and their phenotypes are altered during wound healing. They are reported to contribute to not only inflammatory responses but also tissue remodeling. However, few studies in vocal fold biology have focused on the function of macrophages. The purpose of this study was to investigate macrophage polarization and distribution in injured murine vocal folds. Animal experiments with controls. Unilateral vocal fold stripping was performed on C57BL/6 mice, and larynges were harvested 1, 3, 5, 7, and 14 days postinjury. Immunohistochemical analysis of the vocal fold lamina propria was performed to detect the expression of classically activated (M1) and alternatively activated (M2) macrophage markers (inducible nitric oxide synthase [iNOS] and CD206, respectively) in F4/80 The proportion of F4/80 The main population of injured sites gradually shifted from M1 to M2 marker-positive macrophages in murine vocal folds. However, coexistence of M1 and M2 markers in the same macrophages was observed. Our results suggest that macrophage phenotypes are regulated by complex tissue-derived signals and exhibit dynamic changes during wound healing. NA Laryngoscope, 129:E135-E142, 2019.
Substances chimiques
Lectins, C-Type
0
Mannose Receptor
0
Mannose-Binding Lectins
0
Nitric Oxide Synthase Type II
EC 1.14.13.39
Receptors, Cell Surface
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
E135-E142Subventions
Organisme : Grants-in-Aid for Scientific Research from the Japan Society for the Promotion of Science
Pays : International
Organisme : GSK Japan Research Grant 2016
Pays : International
Informations de copyright
© 2018 The American Laryngological, Rhinological and Otological Society, Inc.