Published online May 26, 2024. doi: 10.4252/wjsc.v16.i5.560
Revised: February 26, 2024
Accepted: April 12, 2024
Published online: May 26, 2024
Processing time: 146 Days and 22.9 Hours
Alveolar bone defects caused by inflammation are an urgent issue in oral implant surgery that must be solved. Regulating the various phenotypes of macrophages to enhance the inflammatory environment can significantly affect the progression of diseases and tissue engineering repair process.
To assess the influence of interleukin-10 (IL-10) on the osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) following their interaction with macrophages in an inflammatory environment.
IL-10 modulates the differentiation of peritoneal macrophages in Wistar rats in an inflammatory environment. In this study, we investigated its impact on the proliferation, migration, and osteogenesis of BMSCs. The expression levels of signal transducer and activator of transcription 3 (STAT3) and its activated form, phos
IL-10-stimulated macrophages underwent polarization to the M2 type through substitution, and these M2 macrophages actively facilitated the osteogenic differentiation of BMSCs. Mechanistically, STAT3 signaling plays a crucial role in the process by which IL-10 influences macrophages. Specifically, IL-10 stimulated the activation of the STAT3 signaling pathway and reduced the macrophage inflammatory response, as evidenced by its diminished impact on the osteogenic differentiation of BMSCs.
Stimulating macrophages with IL-10 proved effective in improving the inflammatory environment and promoting the osteogenic differentiation of BMSCs. The IL-10/STAT3 signaling pathway has emerged as a key regulator in the macrophage-mediated control of BMSCs’ osteogenic differentiation.
Core Tip: This study investigated the mechanism of interleukin-10 (IL-10) affecting macrophages in inflammatory environments, observed the effects of different macrophages on the biological behavior and osteogenic differentiation of bone marrow mesenchymal stem cells, and found that IL-10/signal transducer and activator of transcription 3 signaling plays a crucial role in promoting bone formation by affecting macrophages. This study provides a new strategy for solving the problem of poor osteogenesis in bone defect repair caused by an excessive inflammatory response in clinical work.