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. 2021 Apr 14;9:649277. doi: 10.3389/fcell.2021.649277

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Copyright © 2021 Wang, Wang, Kong, Shi, Wang, Chai, Xu and Kang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Working model of ADM2 promoting the coupling of osteogenesis and angiogenesis during DO through NF-κB/β-catenin and AKT/β-catenin signaling. Under the administration of ADM2, NF-κB signaling is inhibited and AKT signaling is activated, leading to the accumulation and activation of β-catenin in BMSCs. Therefore, the osteogenic differentiation and pro-angiogenic potential of BMSCs are promoted, and the tube formation and cell motility of ECs are enhanced. In conclusion, ADM2 could directly promote osteogenesis and indirectly improve angiogenesis through β-catenin signaling, thus enhancing BMSCs-mediated coupling of osteogenesis and angiogenesis and accelerating bone regeneration during DO. ADM2, adrenomedullin 2. AKT, activate protein kinase B. BMSC, bone marrow mesenchymal stem cell. DO, distraction osteogenesis. EC, endothelial cell. NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells.