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在急性炎症期间,CCL2通过促进巨细胞迁移来促进骨质生成

Masakazu Toya¹, Ning Zhang^1,2, Masanori Tsubosaka¹

¹Department of Orthopaedic Surgery, Stanford University School of Medicine, Stanford, CA, United States.

Frontiers in cell and developmental biology

|July 17, 2023

概括

向C-C动机化学因子连接体2 (CCL2) 与介酶体 stromal 细胞 (MSCs) 和巨细胞的向显示了增强骨愈合的前景. 急性CCL2刺激通过指导巨细胞迁移和促进MSC-巨细胞交叉交流,促进骨质生成.

科学领域:

生物医学工程生物医学工程
再生医学是一种再生医学.
整形外科整形外科整形外科

背景情况:

老年人的复杂骨折和骨缺陷需要新的最小侵入性治疗来实现强大的骨愈合.
使用介质细胞 stromal 细胞 (MSCs) 的局部细胞治疗是一种潜在的策略,利用它们的骨质生和免疫调节作用.
MSC - 巨细胞交叉对骨再生至关重要,C-C动机化学因子连接体2 (CCL2) 影响了这两种细胞类型的迁移.

研究的目的:

调查针对C-C动机化学因配体2 (CCL2) 的治疗潜力,用于骨愈合中的局部细胞疗法.
评估CCL2对MSC骨质分化和MSC-巨相互作用的影响.
评估CCL2过度表达的MSCs在促进骨再生中的作用.

主要方法:

从BALB/c小鼠中分离出MSC和巨细胞.
过度表达CCL2的转基因MSCs是使用lentivirus载体创建的.
骨质分化和细胞迁移测定在MSCs和巨细胞的共同培养中进行,有或没有CCL2刺激.

主要成果:

转基因MSC表现出显著更高的CCL2分泌,而不会影响细胞增殖.
急性CCL2刺激 (1天),但不是持续刺激 (7天),在MSC-巨共同培养中显著增加了骨质分化.
复合CCL2和由MSCs分泌的CCL2都有效地促进了巨细胞的迁移.

结论:

急性CCL2刺激增强MSC-巨共同培养中的骨质生成,这表明在早期炎症阶段的骨愈合中发挥了作用.
CCL2通过指导巨细胞迁移,促进MSC-巨细胞交叉,并可能授权MSC来促进骨愈合.
将CCL2,MSC和巨细胞结合在一起,为治疗受损骨愈合提供了一个有希望的策略.

关键词:

在CCL2中,我们可以使用CCL2.在MCP1中,MCP1是MCP1.我们的MSc是MSc.这是一种炎症炎症炎症炎症.巨细胞是一个巨细胞.移民移民迁移迁移骨质发生过程 (osteogenesis)

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