The "oligovascular unit" is a dynamic structural complex composed of endothelial cells (ECs) and oligodendrocyte progenitor cells (OPCs)/oligodendrocytes. By improving the microenvironment of OPCs in the "oligovascular unit" and promoting the proliferation and differentiation of OPCs, both myelination and white matter injury can be repaired. However, it is unclear what characteristic changes occur in the microenvironment of the "oligovascular unit" after preterm white matter injury (PWMI). Here, we demonstrate the changes in the "oligovascular unit" induced by hypoxia-ischemia (HI) and its underlying mechanism in PWMI mice. White matter injury and inhibited production of myelin from OPCs were observed by histopathological staining in HI neonatal mice. We further observed that the proliferation of OPCs and angiogenesis were increased after HI, which is considered the response of the body and cells to HI. HI-induced oligogenesis occurs around the vessels, indicating that "oligovascular units" exist and promote the proliferation and differentiation of OPCs after HI in the short term. We also determined that angiogenesis and oligogenesis induced by HI in the white matter are related to the PI3K/AKT/mTOR pathway. Furthermore, the myelin sheaths were shown to be disordered on the side of the surgery, and the myelin-dense layer was poorly developed at P14 and P28. Different degrees of damage to the vascular ECs and basement membrane on the surgical side were detected beginning at P4, indicating that EC injury is an early phenomenon that subsequently affects oligogenesis. Taken together, our findings indicate that the proliferation of OPCs and angiogenesis in white matter are increased in the early stage of HI involving PI3K/AKT/mTOR pathway activation. Promoting vascular endothelial function and angiogenesis may increase the proliferation and survival of OPCs via the "oligovascular unit," which suggests a potential method to repair injured white matter in the early stage of PWMI.

中文翻译：

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缺氧缺血性新生小鼠中“寡血管单位”中的成卵涉及PI3K / AKT / mTOR信号传导。

“少血管单位”是由内皮细胞（EC）和少突胶质祖细胞（OPC）/少突胶质细胞组成的动态结构复合物。通过改善“微血管单元”中OPC的微环境并促进OPC的增殖和分化，可以修复髓鞘化和白质损伤。但是，尚不清楚早产白质损伤（PWMI）后“寡血管单位”的微环境中会发生什么特征性变化。在这里，我们证明了缺氧缺血（HI）诱导的“寡血管单位”的变化及其在PWMI小鼠中的潜在机制。在HI新生小鼠中，通过组织病理学染色观察到OPCs的白质损伤和髓磷脂产生受到抑制。我们进一步观察到，HI后OPC的增殖和血管生成增加，这被认为是机体和细胞对HI的反应。HI诱导的寡聚发生在血管周围，表明HI后短期内存在“寡血管单位”并促进OPC的增殖和分化。我们还确定了白质中HI诱导的血管生成和寡聚与PI3K / AKT / mTOR途径有关。此外，在手术一侧，髓鞘鞘显示紊乱，在P14和P28处，髓鞘密集层发育不良。从P4开始检测到对手术侧血管EC和基底膜的不同程度的损伤，表明EC损伤是一种早期现象，随后会影响寡聚物形成。在一起 我们的研究结果表明，在涉及PI3K / AKT / mTOR途径活化的HI早期，OPCs的增殖和白质中的血管生成增加。促进血管内皮功能和血管生成可通过“少血管单元”增加OPC的增殖和存活，这提示了在PWMI早期修复受损白质的潜在方法。