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首页> 外文期刊>Journal of Thoracic Disease >VEGFR endocytosis regulates the angiogenesis in a mouse model of hindlimb ischemia
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VEGFR endocytosis regulates the angiogenesis in a mouse model of hindlimb ischemia

机译：VEGFR内吞作用调节小鼠后肢缺血模型中的血管生成

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Background: The regulation of angiogenesis in the treatment of cardiovascular diseases has been widely studied and the vascular endothelial growth factor (VEGF) families and VEGF receptor (VEGFR) have been proven to be one of the key regulators. The VEGFR endocytosis has been recently proved to be involved in the regulation of angiogenesis. Our previous study showed that the upregulation of VEGFR endocytosis enhanced angiogenesis in vitro . In this research, we utilized mice with induced hindlimb ischemia, as a model to investigate the role of VEGFR endocytosis in the regulation of angiogenesis in vivo . Our goal was to observe the effect of revascularization with different degrees of VEGFR endocytosis after injecting atypical protein kinase C inhibitor (αPKCi) and dynasore, which could respectively promote and inhibit the VEGFR endocytosis. Methods: We induced the hindlimb ischemia in adult male mice by ligating the hindlimb artery. By directly injecting the ischemic muscles with endothelial progenitor cells (EPCs) alone or EPCs + αPKCi/EPCs + dynasore or control medium (sham group), we divided the mice into four groups and detected lower limb blood flow using a laser Doppler blood perfusion imager. We also measured the immunohistochemistry (IHC) of markers for angiogenesis, such as CD31 and alpha smooth muscle actin (α-SMA) in the ischemic hindlimb tissues. Results: We demonstrated VEGFR endocytosis played an important role in the angiogenesis of the ischemic hindlimb model in vivo . By using atypical PKC inhibitor that increase the VEGFR endocytosis, the angiogenesis in the mice model was promoted. Treatment with EPCs + αPKCi showed greater effects on blood perfusion recovery and increased the α-SMA-positive vessels. Conclusions: The regulation of VEGFR endocytosis represents a valuable method of improving angiogenesis and thus revascularization in ischemic disease model.
机译：背景：血管生成在心血管疾病治疗中的调控已被广泛研究，并且血管内皮生长因子（VEGF）家族和VEGF受体（VEGFR）已被证明是关键的调控因子之一。最近已经证明，VEGFR内吞作用与血管生成的调节有关。我们先前的研究表明，VEGFR内吞作用的上调增强了体外血管生成。在这项研究中，我们利用诱发后肢缺血的小鼠作为模型来研究VEGFR内吞作用在体内调节血管生成中的作用。我们的目标是在注射非典型蛋白激酶C抑制剂（αPKCi）和达纳西尔后观察不同程度VEGFR内吞作用对血运重建的影响，这可以分别促进和抑制VEGFR内吞作用。方法：通过结扎后肢动脉，诱导成年雄性小鼠后肢缺血。通过直接用单独的内皮祖细胞（EPC）或EPC +αPKCi/ EPC + dynasore或对照培养基（假手术组）直接注射缺血肌肉，将小鼠分为四组，并使用激光多普勒血流灌注成像仪检测下肢血流。我们还测量了缺血后肢组织中血管生成标记（例如CD31和α平滑肌肌动蛋白（α-SMA））的免疫组织化学（IHC）。结果：我们证明了VEGFR内吞作用在体内缺血后肢模型的血管生成中起着重要作用。通过使用增加VEGFR内吞作用的非典型PKC抑制剂，促进了小鼠模型中的血管生成。 EPCs +αPKCi的治疗对血液灌注恢复具有更大的影响，并增加了α-SMA阳性血管。结论：VEGFR内吞作用的调节是改善血管生成从而改善缺血性疾病模型中血管重建的一种有价值的方法。

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