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主要人类肺纤维细胞的刺激特异衰老调节膜干细胞功能

Maria Camila Melo-Narváez^1,2, Nora Bramey¹, Fenja See¹

¹Institute of Lung Health and Immunity (LHI), Helmholtz Munich, Comprehensive Pneumology Center (CPC-M), German Center for Lung Research (DZL), 81377 Munich, Germany.

|July 12, 2024

概括

肺纤维细胞中的细胞衰老在慢性肺病 (CLD) 中增加,例如异常性肺纤维化 (IPF) 和慢性阻塞性肺病 (COPD). 不同的触发因素会诱导不同的衰老,损害肺前代细胞的功能.

科学领域:

细胞和分子生物学细胞和分子生物学
衰老研究研究衰老研究
肺部医学肺部医学

背景情况:

衰老是慢性肺病 (CLD) 的主要危险因素,包括异常性肺纤维化 (IPF) 和慢性阻塞性肺病 (COPD).
细胞衰老是衰老的标志,在CLD患者的肺细胞中升高.
触发因素和衰老在CLD病原发生中的特定作用仍然不清楚.

研究的目的:

来自对照,IPF和COPD患者的初级人类肺纤维细胞 (phLF) 的衰老特征.
研究疾病相关的侮辱 (H2O2,白血素,TGF-β1) 如何诱导phLF的衰老.
通过器官模型评估衰老对肺前代细胞潜力的影响.

主要方法:

从对照组,IPF和COPD捐赠者的初级人类肺纤维细胞 (phLF) 在基线和暴露于H2O2,白素或TGF-β1.1后被分析.
大量RNA测序用于表征转录变化.
肺器官模型被用来评估老化phLF对膜上皮质前代细胞功能的影响.

主要成果:

来自IPF和COPD患者的phLF表现出不同的基线转录程序,但具有共同的衰老表型.
H2O2和白素,但不是TGF-β1,在疾病组中诱导了phLF的衰老.
诱导衰老导致独特的衰老相关分泌表型 (SASP),具体取决于触发因素.
衰老的phLF (来自白素和H2O2治疗) 降低了共培养中膜上皮原体原生细胞的原生能力.

结论:

从COPD和IPF患者的肺纤维细胞共享一个保存的衰老反应.
衰老表型及其后果取决于具体的侮辱.
肺纤维细胞的衰老损害了膜上皮原生细胞的再生潜力ex vivo.

关键词:

衰老的衰老衰老的衰老细胞衰老细胞衰老慢性肺部疾病慢性肺部疾病纤维细胞的细胞.

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