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带有肺高血压的支气管肺功能失生症与塞马福林信号的丧失以及FOXF1表达的功能性下降有关

Shawyon P Shirazi, Nicholas M Negretti, Christopher S Jetter

bioRxiv : the preprint server for biology

|September 10, 2024

概括

婴儿肺部损伤可以导致支气管肺功能失调 (BPD) 和肺高血压 (PH). 这项研究揭示了BPD肺部异常的毛细血管细胞和半波林信号缺陷,将BPD和膜毛细血管形症联系起来.

科学领域:

新生儿呼吸道医学新生儿呼吸道医学
分子生物学分子生物学
发育生物学是发展生物学.

背景情况:

婴儿肺部损伤可能导致支气管肺部发育不良 (BPD),这是一种与结构和功能呼吸系统缺陷相关的疾病.
严重的BPD可以发展为肺高血压 (PH),影响婴儿的健康结果.
了解推动BPD进展的细胞和分子机制对于开发有效治疗非常重要.

研究的目的:

调查早产婴儿发展的支气管肺功能障碍症 (BPD) 的细胞和分子动态.
为了比较婴儿的肺组织与早期BPD和BPD与肺高血压 (PH) 的婴儿的肺组织.
为了确定关键的分子通路和细胞状态,涉及到BPD的发病.

主要方法:

单细胞RNA测序是在从BPD/BPD+PH的早产婴儿和到期婴儿的肺组织样本上进行的.
分析了内皮细胞状态,以确定异常细胞群.
用预测信号通路分析来识别分子缺陷.
用于验证的是小鼠BPD模型和患有膜毛细管发育不良 (ACDMPV) 的人类样本.

主要成果:

在患有BPD和PH的婴儿中,发现了一个独特的异常毛细血管细胞状态,其特征是 *ANKRD1* 表达,在婴儿中发现了异常毛细血管细胞状态.
在患有BPD/BPD+PH的婴儿的膜膜上观察到塞马福林指导-提示信号通路的缺陷.
在BPD/BPD+PH肺样本中发现了亲血管性转录因子*FOXF1*的表达减少.
在小鼠BPD模型和人类ACDMPV病例中复制了塞马福林信号的损失.

结论:

异常的毛细血管细胞状态和半波林信号通路缺陷是早产婴儿BPD的关键特征.
塞马福林信号传递在正常肺部发育中起着至关重要的作用,并且可能与BPD和ACDMPV有机联系.
这些发现为BPD和ACDMPV的基础发展计划提供了洞察力,并建议潜在的治疗点.

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