摘要
Toll样受体(TLR)4是人类发现的第一个TLR相关蛋白质,主要介导格兰阴性细菌的免疫过程。TLR2具有相对广泛的配体特异性,可识别多种病原体相关分子模式,协助TLR4参与人体内对脂多糖的反应。研究显示,TLR2和TLR4参与多种细胞成骨向分化的调控。譬如TLR2和TLR4即可通过促进主动脉瓣间质细胞的成骨向分化参与主动脉瓣钙化过程,也可通过上调冠状动脉内皮细胞中骨形态发生蛋白2的表达参与冠状动脉粥样硬化,还可参与骨髓间质干细胞的成骨向分化。在牙髓组织中,有TLR4表达的成牙本质细胞样细胞可向成牙本质细胞受损处迁移并形成修复性牙本质;而TLR2和TLR4作为参与牙髓防御反应的成员,在牙髓组织受损时,不仅可调节炎症因子的表达,还参与牙髓细胞成牙本质向分化的调控。由此可见,TLR2和TLR4在细胞成骨向分化中的作用机制值得进一步的探讨。
Toll-like receptor（TLR） 4, which mediates immunity to grand negative bacteria, is the first-identified TLR family member. TLR2 recognizes many pathogen-associated molecular patterns and responds to lipopolysaeeharide stimuli with TLR4. TLR2 and TLR4 have been confirmed to regulate the osteogenesis of some ceils. For example, TLR2 and TLR4 participate in aortic valve calcification through the upregulation of osteogenic differentiation in human aortic valve interstitial cells. TLP,2 and TLR4 can also improve coronary atherosclerosis by increasing the expression of bone morphogenetic protein 2 in coronary artery endothelial cells, and they are involved in the osteogenic differentiation of bone marrow stromal cells. In dental pulp tissue, odontoblast-like cells, which express TLR4, migrate to damaged zones of odontoblasts and form reparative dentin. Both TLR2 and TLR4 regulate the expression of inflammation factors and odontoblastic differentiation when damage occurs. Thus, the regulation mechanism of TLR2 and TLR4 in osteogenie differentiation needs to be studied further.
出处
《国际口腔医学杂志》
CAS
北大核心
2015年第4期492-495,共4页
International Journal of Stomatology
基金
卫生部临床学科重点项目(2010439)
