[E2 signaling in myofibers promots macrophage efferocytosis in mouse skeletal muscles with cardiotoxin-induced acute injury].
Year: 2024
Type: other
Abstract: OBJECTIVE: signaling in myofibers on muscular macrophage efferocytosis in mice with cardiotoxin-induced acute skeletal muscle injury. METHODS: of the mice were detected using ELISA, and the number, phenotypes, and efferocytosis of the macrophages in the inflammatory exudates and myofiber regeneration and repair were evaluated using immunofluorescence staining and flow cytometry. C2C12 cells were induced to differentiate into mature myotubes, which were treated with IFN- γ for 24 before treatment with β -Estradiol or 4-OHT. The treated myotubes were co-cultured with mouse peritoneal macrophages in a 1:2 ratio, followed by addition of PKH67-labeled apoptotic mouse mononuclear spleen cells induced by UV irradiation, and macrophage efferocytosis was observed using immunofluorescence staining and flow cytometry. RESULTS: Compared with the control mice, the female mice with ovariectomy showed significantly increased mononuclear macrophages in the inflammatory exudates, with increased M1 cell percentage, reduced M2 cell percentage and macrophage efferocytosis in the injured muscle, and obviously delayed myofiber regeneration and repair. In the cell co-culture systems, treatment of the myotubes with β-estradiol significantly increased the number and proportion of M2 macrophages and macrophage efferocytosis, while 4-OHT treatment resulted in the opposite changes. CONCLUSION: signaling promotes M1 to M2 transition to increase macrophage efferocytosis, thereby relieving inflammation and promoting muscle regeneration and repair.
Source: PubMed
Institutions: Foshan University, Southern Medical University
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W4405028485