基质刚性和粘性影响纤维细胞衰老
bioRxiv : the preprint server for biology
|September 5, 2025
概括
组织机制影响细胞衰老. 软,粘弹性材料可以在纤维细胞中诱导衰老,即使没有DNA损伤,这突显了材料特性在衰老和纤维化中的作用.
科学领域:
- 生物材料科学
- 细胞生物学
- 组织工程
背景情况:
- 细胞衰老与衰老和纤维化有关,
- 机械力量对衰老诱导的直接影响尚未完全理解.
- 纤维细胞在组织结构中发挥关键作用,并与纤维细胞疾病有关.
研究的目的:
- 研究水凝硬度和粘性如何影响纤维细胞衰老.
- 为了确定单独的机械特性是否能诱导衰老.
- 探索YAP信号和核组织在机械诱导衰老中的作用.
主要方法:
- 使用了具有不同刚度 (kPa范围) 和粘弹性特性的水凝.
- 暴露在这些水凝中的人类肺纤维细胞,有或没有基因毒性压力.
- 分析了纤维细胞衰老标志物,YAP局部化和核形态 (DAPI强度).
主要成果:
- 衰老的纤维细胞保留了机械感知,在更硬的水凝上显示了YAP核定位的增加.
- 软 (2kPa) 粘弹性基板单独诱导和放大衰老,独立于基因毒性应激.
- 机械诱导的衰老与核DAPI强度的下降有关,而不是YAP活动的下降.
结论:
- 水凝的粘性,特别是软基质,在诱导纤维细胞衰老方面发挥着重要作用.
- 细胞机械感知和核组织对于机械线索的反应至关重要.
- 这项研究强调了材料特性在细胞衰老和纤维化疾病发展中的重要性.
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