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基质硬度通过调节12-脂氧合酶介导的早期炎症反应来调控骨修复。

Matrix stiffness regulates bone repair by modulating 12-lipoxygenase-mediated early inflammation.

作者信息

Yao Dongdong, Qiao Fangyu, Song Chenchen, Lv Yonggang

机构信息

Mechanobiology and Regenerative Medicine Laboratory, Bioengineering College, Chongqing University, Chongqing 400044, PR China.

Mechanobiology and Regenerative Medicine Laboratory, Bioengineering College, Chongqing University, Chongqing 400044, PR China.

出版信息

Mater Sci Eng C Mater Biol Appl. 2021 Sep;128:112359. doi: 10.1016/j.msec.2021.112359. Epub 2021 Aug 8.

Abstract

Lipid metabolism in macrophages has been increasingly emphasized in exerting an anti-inflammatory effect and accelerating fracture healing. 12-lipoxygenase (12-LOX) is expressed in several cell types, including macrophages, and oxidizes polyunsaturated fatty acids (PUFAs) to generate both pro- and anti-inflammatory lipid mediators, of which the n-3 PUFAs play an important part in tissue homeostasis/fibrosis. Although mechanical factor regulates the lipid metabolic axis of inflammatory cells, specifically matrix stiffness influences macrophages metabolic responses, little is known about how matrix stiffness affects the 12-LOX-mediated early inflammation in bone repair. In the present study, demineralized bone matrix (DBM) scaffolds with different matrix stiffness were constructed by controlling the duration of decalcification (0 h (control), 1 h (high), 12 h (medium), and 5 d (low)) to repair the defected rat skull. The expression of inflammatory cytokines and macrophages polarization were analyzed. The lipid metabolites and lipid mediators' biosynthesis by matrix stiffness-regulated were further detected. The results showed that the low matrix stiffness could polarize macrophages into an anti-inflammatory phenotype, promote the expression of anti-inflammatory cytokines and specialized pro-resolving lipid mediators (SPMs) biosynthesis beneficial for the osteogenesis of mesenchymal stem cells (MSCs). After treated with ML355, the expression of anti-inflammatory cytokines/proteins and SPMs biosynthesis in macrophages cultured on low-matrix stiffness scaffolds were repressed, and there were almost no statistical differences among all groups. Findings from this study support that matrix stiffness regulates bone repair by modulating 12-LOX-mediated early inflammation, which suggest a direct mechanical impact of matrix stiffness on macrophages lipid metabolism and provide a new insight into the clinical application of SPMs for bone regeneration.

摘要

巨噬细胞中的脂质代谢在发挥抗炎作用和加速骨折愈合方面的重要性日益凸显。12-脂氧合酶(12-LOX)在包括巨噬细胞在内的多种细胞类型中表达,可氧化多不饱和脂肪酸(PUFA)以生成促炎和抗炎脂质介质,其中n-3多不饱和脂肪酸在组织稳态/纤维化中起重要作用。尽管机械因素调节炎症细胞的脂质代谢轴,特别是基质硬度影响巨噬细胞的代谢反应,但关于基质硬度如何影响骨修复中12-LOX介导的早期炎症知之甚少。在本研究中,通过控制脱钙时间(0小时(对照)、1小时(高)、12小时(中)和5天(低))构建具有不同基质硬度的脱矿骨基质(DBM)支架,以修复大鼠颅骨缺损。分析了炎症细胞因子的表达和巨噬细胞极化情况。进一步检测了基质硬度调节的脂质代谢产物和脂质介质的生物合成。结果表明,低基质硬度可使巨噬细胞极化为抗炎表型,促进抗炎细胞因子的表达以及对间充质干细胞(MSC)成骨有益的特异性促消退脂质介质(SPM)的生物合成。用ML355处理后,在低基质硬度支架上培养的巨噬细胞中抗炎细胞因子/蛋白的表达和SPM的生物合成受到抑制,且各组之间几乎没有统计学差异。本研究结果支持基质硬度通过调节12-LOX介导的早期炎症来调节骨修复,这表明基质硬度对巨噬细胞脂质代谢有直接的机械影响,并为SPM在骨再生中的临床应用提供了新的见解。

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