表皮多细胞聚类是通过在软矩阵上的极化巨细胞来实现的
Hannah Zmuda1, Amit Pathak1,2
1Department of Biomedical Engineering, Washington University, St. Louis, Missouri, USA.
概括
免疫细胞和矩阵刚度极大地调节了上皮细胞的聚类. 在软基质上,M1的炎症性巨细胞促进上皮质的聚合,这对组织修复和瘤生长至关重要.
科学领域:
- 生物医学工程 生物医学工程
- 细胞生物学 细胞生物学
- 免疫学 免疫学 免疫学
背景情况:
- 表皮结构的形成对于器官生成,瘤生长和伤口修复至关重要.
- 免疫细胞和微环境机械线索对上皮细胞聚类的影响仍然不太清楚.
研究的目的:
- 为了研究免疫细胞 (巨细胞) 和矩阵刚性如何影响人类乳腺上皮细胞聚类.
- 阐明了表皮形态发生的巨介导调节的分子机制.
主要方法:
- 人类乳腺上皮细胞与M0,M1或M2巨细胞共同培养在软或硬的水凝上.
- 对上皮细胞迁移,聚类,焦点粘附,纤维内素沉积和非肌肉肌-IIA表达的分析.
- 评估细胞因子分泌 (TNF-α,TGF-β) 和ROCK抑制和外源TGF-β的影响.
主要成果:
- 与M0或M2巨相比,在软矩阵上的M1巨显著增强了上皮细胞迁移和多细胞聚类.
- 刚性矩阵通过增加细胞迁移和细胞-细胞外矩阵粘附来抑制上皮质聚类.
- 带有M1巨细胞的软矩阵调节了焦点粘附,纤维菌素和非肌肉髓-IIA,促进了依赖细胞力量 (ROCK通路) 的聚类.
- 巨细胞分泌的因素,特别是TGF-β,影响了上皮质聚类.
结论:
- 微环境的机械性质和免疫细胞两极分化都是上皮细胞聚类的关键调节者.
- 了解这些相互作用可以为调节组织修复,纤维化和瘤进展的策略提供信息.
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