骨细胞连接蛋白 43 通道影响骨折愈合。
Osteocytic connexin 43 channels affect fracture healing.
机构信息
Key Laboratory for Space Bioscience and Biotechnology, School of Life Sciences, Northwestern Polytechnical University, Xi'an, Shaanxi, China.
Key Laboratory for Space Bioscience and Biotechnology, Research & Development Institute in Shenzhen, Northwestern Polytechnical UniversityShenzhen, Shenzhen, Guangdong, China.
出版信息
J Cell Physiol. 2019 Nov;234(11):19824-19832. doi: 10.1002/jcp.28581. Epub 2019 Apr 13.
The cross-talk between cells is very critical for moving forward fracture healing in an orderly manner. Connexin (Cx) 43-formed gap junctions and hemichannels mediate the communication between adjacent cells and cells and extracellular environment. Loss of Cx43 in osteoblasts/osteocytes results in delayed fracture healing. For investigating the role of two channels in osteocytes in bone repair, two transgenic mouse models with Cx43 dominant negative mutants driven by a 10 kb-DMP1 promoter were generated: R76W (gap junctions are blocked, whereas hemichannels are promoted) and Δ130-136 (both gap junctions and hemichannels are blocked). R76W mice (promotion of hemichannels) showed a significant increase of new bone formation, whereas delayed osteoclastogenesis and healing was observed in Δ130-136 (impairment of gap junctions), but not in R76W mice (hemichannel promotion may recover the delay). These results suggest that gap junctions and hemichannels play some similar and cooperative roles in bone repair.
细胞间的串扰对于有序地推进骨折愈合非常关键。连接蛋白 (Cx) 43 形成的缝隙连接和半通道介导相邻细胞以及细胞与细胞外环境之间的通讯。成骨细胞/成骨细胞中 Cx43 的缺失导致骨折愈合延迟。为了研究骨细胞中这两种通道在骨修复中的作用，使用由 10 kb-DMP1 启动子驱动的 Cx43 显性负突变体生成了两种转基因小鼠模型：R76W（缝隙连接被阻断，而半通道被促进）和 Δ130-136（缝隙连接和半通道均被阻断）。R76W 小鼠（半通道促进）表现出显著增加的新骨形成，而 Δ130-136 小鼠（缝隙连接受损）则出现成骨细胞生成延迟和愈合，而在 R76W 小鼠（半通道促进可能恢复延迟）中则没有观察到这种情况。这些结果表明，缝隙连接和半通道在骨修复中发挥一些相似且协同的作用。
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