流体剪切力作用下间隙连接蛋白Cx43在骨改建中的机制初探  

Preliminary Study on the Mechanism of Gap Junction Protein Cx43 in Bone Remodeling Under Fluid Shearforce

作　　者：李晓婷 Li Xiaoting(Chengdu Women and Children s Hospital Affiliated to the School of Medicine,Chengdu Women and Children s Central Hospital,Chengdu,Sichuan 610031,China)

机构地区：[1]电子科技大学医学院附属妇女儿童医院·成都市妇女儿童中心医院,四川成都610031

出　　处：《四川医学》2023年第1期23-27,共5页Sichuan Medical Journal

摘　　要：目的 探讨骨细胞在受到机械流体剪切力作用后,间隙连接蛋白Cx43参与骨改建的机制。方法 将受流体剪切力作用的骨细胞分成5组,即施加生理流体剪切力组,过大流体剪切力组,siRNA干扰组,18a-GA阻断组,对照组。收集加力后系统内的循环液体作为条件培养基对单核细胞株RAW264.7和骨髓间充质干细胞MSCs进行培养,观察破骨细胞的生成和钙化结节形成情况。结果 抑制骨细胞内Cx43的表达或阻断胞间的间隙连接通路,均能导致破骨细胞诱导生成相关因子增加,促进破骨细胞生成,抑制骨髓间充质干细胞MSCs成骨向分化。结论 间隙连接蛋白Cx43作为骨细胞上的力学感应受体,能通过影响成骨、破骨活动对骨改建发挥重要的调节作用。Objective To investigate the mechanism of connexin Cx43 involved in bone resorption and remodeling when osteocytes were exposed to mechanical fluid shear stress. Methods Osteocytes exposed to mechanical fluid shear stress were cultured in five groups: physiological fluid shear force, excessive fluid shear force, siRNA interference group, 18a-GA blocking group and control group. Bone marrow mesenchymal stem cells(MSCs)and RAW264.7 were cultured in circulation fluid of these five groups. The formation of osteoclasts and calcified nodules were observed. Results Inhibiting the expression of Cx43 in cells or blocking the gap junction pathway between cells could increase the related factors which promoted osteoclast formation, and inhibit the osteogenic differentiation of MSCs. Conclusion Cx43,as mechanical receptors on bone cells, could play an important role in regulating bone remodeling by affecting osteogenesis and osteoclast activity.

关 键 词：流体剪切力 骨细胞 connexin 43 骨改建 

分 类 号：R336[医药卫生—人体生理学]