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炎症性巨细胞分泌的细胞因子调节膜间歇细胞中的性别差异在水凝生物材料上

Nicole E Félix Vélez^1,2, Kristi Tu^1,2, Peng Guo³

¹Shu Chien-Gene Lay Department of Bioengineering, University of California, San Diego, California, USA.

Journal of biomedical materials research. Part A

|February 25, 2025

概括

大动脉狭窄 (AVS) 中的炎症对男性和女性的影响不同. 瘤亡因子-α驱动女性肌纤维细胞激活,而男性通过其他途径显示失活,突出性别特异性的细胞反应.

科学领域:

心血管生物学心血管生物学
生物材料科学生物材料科学
细胞信号传输细胞信号传输

背景情况:

大动脉缩症 (AVS) 涉及膜纤维化和化,可能导致心力衰竭.
由亲炎性巨细胞的细胞因子驱动的炎症,通过激活膜间歇细胞 (VICs) 进入肌纤维细胞,与AVS有关.
根据生物性别,炎症性细胞因子如何影响肌纤维细胞激活的精确分子机制尚不清楚.

研究的目的:

为了研究炎症性细胞因子对VIC激活到肌纤维细胞和骨质细胞样细胞的性别特异性影响.
使用体外水凝培养平台培养雄性和雌性VICs.
阐明涉及到AVS中性别依赖细胞反应的分子途径.

主要方法:

开发一个体外水凝培养平台.
男性和女性膜间歇细胞 (VICs) 的培养.
细胞因子诱导的VIC激活和分化的特征.

主要成果:

瘤坏死因子-α (TNF-α) 通过MAPK/ERK信号传递,染色质可用性和通过RUNX2核定位的骨质细胞样分化诱导女性特异性肌纤维细胞激活.
观察到针对TNF-α的男性特异性肌纤维细胞失活,通过独立于MAPK/ERK信号传递的途径发生.
水凝生物材料在区分性别特异性细胞表型方面被证明是有效的.

结论:

在AVS的背景下,VIC对TNF-α等炎症刺激的反应存在显著的性别差异.
MAPK/ERK信号传递和RUNX2核定位是女性特异性VIC激活和分化的关键媒介.
另一种信号通路参与了男性特异性的VIC禁用,这需要进一步调查.
先进的细胞培养平台对于揭示心血管疾病中的性别特异性生物机制至关重要.

关键词:

石灰化是指化.纤维化纤维化这种水凝是水凝.这是一种炎症炎症炎症炎症.巨细胞是什么?巨细胞是什么?肌纤维母细胞细胞.性别差异的性别差异.

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