Research on the regulation of macrophage polarization by parathyroid hormone in an inflammatory microenvironment to promote osteogenic differentiation of osteoblasts
10.3969/j.issn.1001-3733.2025.06.002
- VernacularTitle:甲状旁腺激素在炎性微环境下调控巨噬细胞极化促进成骨细胞成骨分化的研究
- Author:
Liyue TIAN
1
;
Yiheng LIU
1
;
Yongdi LI
1
;
Duchenhui LI
1
;
Zhishan YANG
1
;
Zhenglong TANG
1
Author Information
1. 550004 贵阳,贵州医科大学附属口腔医院口腔颌面外科
- Publication Type:Journal Article
- Keywords:
Parathyroid hormone;
miR-155-5p;
Macrophage;
Osteoblast;
Osteanagenesis
- From:
Journal of Practical Stomatology
2025;41(6):737-743
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To explore the effects of parathyroid hormone(PTH)on the osteogenic differentiation of osteoblasts by reg-ulating macrophage polarization in inflammatory microenvironment.Methods:Macrophages were pretreated with lipopolysaccharide(LPS)for 2 h to establish an inflammatory microenvironment model,and then treated with PTH for 24 h.Macrophages and osteo-blasts were co-cultured in Transwell cells.Alkaline phosphatase staining,alizarin red staining,RT-qPCR and Western blot were applied to detect osteogenic differentiation.The expression of SOCS1/JAK2/STAT3 protein in macrophages was detected by West-ern blot.The change of STAT3 expression was detected after adding AG490.The expression of miR-155-5p,SOCS1,IL-1β,IL-6 and i-NOS was detected by ELISA and RT-qPCR.Results:LPS induced M1-type polarization of macrophages and inhibited the osteogenic differentiation of osteoblasts.PTH inhibited the polarization of M1-type macrophages and promoted the osteogenic differ-entiation of osteoblasts in inflammatory microenvironment(P＜0.05).PTH down-regulated the expression of miR-155-5p,IL-1β,IL-6,i-NOS,p-JAK2/JAK2 and p-STAT3/STAT3 in macrophages under inflammatory microenvironment(P＜0.05),and up-reg-ulated SOCS1(P＜0.05).AG490 further inhibited p-STAT3/STAT3 expression.Conclusion:PTH inhibits the polarization of M1-type macrophages and promotes osteogenic differentiation of osteoblasts by down-regulating miR-155-5p and then targeting SOCS1/JAK2/STAT3 signaling pathway in inflammatory microenvironment.
