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首页> 外文期刊>Cell and Tissue Research >Requirement of Runx3 in pulmonary vasculogenesis.
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Requirement of Runx3 in pulmonary vasculogenesis.

机译：Runx3在肺血管生成中的需求。

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Runx3 is essential for normal vertebrate lung development and Runx3 knockout (KO) mice die within 24 h after birth because of various organ defects including defects in alveolar expansion. For proper early lung development, vasculogenesis and angiogenesis are necessary in humans. Previous studies have reported that various signaling molecules, such as CD31, VEGF and vWF, are closely related to lung vasculogenesis and angiogenesis. To confirm the relationship between Runx3-related lung defects and vasculogenesis, the localization of various blood vessel markers is examined in WT and Runx3 KO mouse lungs at PN1. Our results indicate that CD31, VEGF and vWF were dramatically up-regulated by a loss of Runx3 during lung development. Moreover, U0126, a MEK inhibitor, rescued the lung phenotype and vascularization by regulation of ERK signaling. Therefore, it was concluded that lung vasculogenesis and angiogenesis were induced in the Runx3 KO mouse, which shows lung defects, by increased CD31, VEGF and vWF.
机译：Runx3对于正常的脊椎动物肺发育至关重要，Runx3基因敲除（KO）小鼠在出生后24小时内会死亡，这是由于各种器官缺陷（包括肺泡扩张缺陷）导致的。为了适当地早期肺发育，人类中血管生成和血管生成是必需的。先前的研究已报道各种信号分子，例如CD31，VEGF和vWF与肺血管生成和血管生成密切相关。为了确认Runx3相关的肺缺陷与血管生成之间的关系，在WT1和Runx3 KO小鼠肺的PN1处检查了各种血管标记的定位。我们的结果表明，在肺发育过程中，Runx3的缺失显着上调了CD31，VEGF和vWF。此外，MEK抑制剂U0126通过调节ERK信号传导拯救了肺表型和血管形成。因此，可以得出结论，通过增加CD31，VEGF和vWF，在Runx3 KO小鼠中诱导了肺血管生成和血管生成，显示出肺部缺陷。

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