After epiphyseal fracture, the epiphyseal plate is prone to ischemia and hypoxia, leading to the formation of bone bridge and deformity. However, the exact mechanism controlling the bone bridge formation remains unclear. Notch/RBPJ signaling axis has been indicated to regulate angiogenesis and osteogenic differentiation. Our study aims to investigate the mechanism of bone bridge formation after epiphyseal plate injury, and to provide a theoretical basis for new therapeutic approaches to prevent the bone bridge formation. The expression of DLL4 and RBPJ was significantly up-regulated in HUVECs after ischemia and hypoxia treatment. Notch/RBPJ pathway positively regulated the osteogenic differentiation of BMSCs. HUVECs can induce osteogenic differentiation of BMSCs under ischemia and hypoxia. Notch/RBPJ pathway is involved in the regulation of the trans-epiphyseal bridge formation. Notch/RBPJ in HUVECs is associated with osteogenic differentiation of BMSCs and may participate in the regulation of the bone bridge formation across the epiphyseal plate.

中文翻译：

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缺氧环境通过激活HUVECs中Notch/RBPJ信号通路促进血管生成和骨桥形成

骨骺骨折后，骨骺板容易缺血缺氧，导致骨桥形成和畸形。然而，控制骨桥形成的确切机制仍不清楚。 Notch/RBPJ 信号轴已被证明可调节血管生成和成骨分化。本研究旨在探讨骨骺板损伤后骨桥形成的机制，为预防骨桥形成的新治疗方法提供理论依据。缺血缺氧处理后HUVECs中DLL4和RBPJ的表达显着上调。 Notch/RBPJ通路正向调节BMSCs的成骨分化。 HUVECs在缺血缺氧条件下可以诱导BMSCs成骨分化。 Notch/RBPJ 通路参与跨骨骺桥形成的调节。 HUVEC 中的 Notch/RBPJ 与 BMSC 的成骨分化相关，可能参与骨骺板骨桥形成的调节。