The role and mechanism of β-catenin-mediated skeletal muscle satellite cells in osteoporotic fractures by Jian-Pi-Bu-Shen formula

IF 2.9 4区生物学 Q3 CELL BIOLOGY

Journal of Molecular Histology Pub Date : 2024-08-06 DOI:10.1007/s10735-024-10238-w

Yanghua Tang, Zhuosong Mu, Dong Pan, Renqi Liu, Shenghu Hong, Zhenfei Xiong

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引用次数: 0

Abstract

Osteoporosis is a metabolic bone disease. β-Catenin is associated with fractures. Jian-Pi-Bu-Shen (JPBS) can promote the healing of osteoporotic fractures (OPF). However, the mechanism of β-catenin-mediated skeletal muscle satellite cells (SMSCs) in OPF by the JPBS is unclear. SMSCs were isolated and divided into five groups. The results showed that the survival rate of SMSCs was significantly higher in the low, medium, and high dose JPBS-containing serum groups after 7 days of incubation. The ALP activity and the number of SMSCs mineralized in the JPBS-containing serum intervention group were elevated. Axin, GSK-3β, β-catenin siRNAs were constructed and transfected into cells. Transfection of siRNAs reduced Axin, GSK-3β, and β-catenin expressions, respectively. β-Catenin-siRNA reversed ALP activity, the number of SMSCs mineralized, and the expression of β-catenin, BMP2, Runx2, COL-I, SP7/Ostrix, Osteocalcin, and BMP-7. Transcriptomic results suggested that the TNF signaling pathway associated with OPF was enriched. SD rats were subjected to the construction of OPF model by removing the ovaries. JPBS decreased the levels of PINP, ALP, CTX, and NTX through β-catenin in OPF rats, while increasing Runx2, β-catenin expressions through β-catenin at the broken end of fractures. Moreover, JPBS decreased BMC, BMD, and BV/TV and improved pathological damage through β-catenin in OPF rats. JPBS decreased the expression of Axin, GSK-3β mRNA, and protein, but increased the expressions of β-catenin, Pax7, COL-II, COL-II, BMP2, and Runx2 through β-catenin in OPF rats. In conclusion, JPBS inhibits Axin/GSK-3β expression, activates the β-catenin signaling, and promotes the osteogenic differentiation of SMSCs.

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简-皮-布-申公式：β-catenin介导的骨骼肌卫星细胞在骨质疏松性骨折中的作用及机制

骨质疏松症是一种代谢性骨病。β-Catenin与骨折有关。健脾益气汤（JPBS）可促进骨质疏松性骨折（OPF）的愈合。然而，健脾益肾汤对β-catenin介导的骨骼肌卫星细胞（SMSCs）在OPF中的作用机制尚不清楚。研究人员分离并将 SMSCs 分成五组。结果表明，培养 7 天后，低、中、高剂量含 JPBS 血清组的 SMSCs 存活率明显较高。含JPBS血清干预组的ALP活性和矿化的SMSCs数量均升高。构建Axin、GSK-3β和β-catenin siRNA并转染细胞。转染 siRNAs 后，Axin、GSK-3β 和 β-catenin 的表达量分别下降。β-catenin-siRNA逆转了ALP活性、矿化的SMSCs数量以及β-catenin、BMP2、Runx2、COL-I、SP7/Ostrix、Osteocalcin和BMP-7的表达。转录组结果表明，与 OPF 相关的 TNF 信号通路得到了丰富。通过切除SD大鼠的卵巢，构建OPF模型。JPBS通过β-catenin降低了OPF大鼠PINP、ALP、CTX和NTX的水平，同时通过β-catenin增加了骨折断端Runx2和β-catenin的表达。此外，JPBS通过β-catenin降低了OPF大鼠的BMC、BMD和BV/TV，并改善了病理损伤。JPBS 降低了 OPF 大鼠 Axin、GSK-3β mRNA 和蛋白的表达，但通过 β-catenin 增加了 β-catenin、Pax7、COL-II、COL-II、BMP2 和 Runx2 的表达。总之，JPBS可抑制Axin/GSK-3β的表达，激活β-catenin信号转导，促进SMSCs的成骨分化。

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来源期刊

Journal of Molecular Histology 生物-细胞生物学

CiteScore

5.90

自引率

0.00%

发文量

审稿时长

1 months

期刊介绍： The Journal of Molecular Histology publishes results of original research on the localization and expression of molecules in animal cells, tissues and organs. Coverage includes studies describing novel cellular or ultrastructural distributions of molecules which provide insight into biochemical or physiological function, development, histologic structure and disease processes. Major research themes of particular interest include: - Cell-Cell and Cell-Matrix Interactions; - Connective Tissues; - Development and Disease; - Neuroscience. Please note that the Journal of Molecular Histology does not consider manuscripts dealing with the application of immunological or other probes on non-standard laboratory animal models unless the results are clearly of significant and general biological importance. The Journal of Molecular Histology publishes full-length original research papers, review articles, short communications and letters to the editors. All manuscripts are typically reviewed by two independent referees. The Journal of Molecular Histology is a continuation of The Histochemical Journal.