Yuan Xingyu, Duan Xianlan, Li Zhao, Yao Bin, Song Wei, Wang Yuzhen, Kong Yi, Zhu Shijun, Zhang Fanliang, Liang Liting, Zhang Mengde, Zhang Chao, Kong Deling, Zhu Meifeng, Huang Sha, Fu Xiaobing
School of Medicine, Nankai University, 94 Weijin Road, Tianjin, 300071, PR China.
Research Center for Tissue Repair and Regeneration Affiliated to the Medical Innovation Research Department, PLA General Hospital, 28 Fuxing Road, Beijing, 100853, PR China.
Bioact Mater. 2022 Sep 14;21:340-357. doi: 10.1016/j.bioactmat.2022.08.021. eCollection 2023 Mar.
The incorporation of vasculature is known to be effective in tissue or organ functional regeneration. However, a vague understanding of the interaction between epidermal appendages and their vascular niches is a foremost obstacle to obtaining sweat gland (SG)-specific vasculature units. Here, we map their precise anatomical connections and report that the interplay between SG cells (SGCs) and the surrounding vascular niche is key for glandular development and homeostasis maintenance. To replicate this interplay , we used three-dimensional (3D) bioprinting to generate reproducible SGC spheroids from differentiated adipose-derived mesenchymal stem cells (ADSCs). With dermal microvascular endothelial cells (DMECs), sacrificial templates made from poly (ε-caprolactone) (PCL) were fabricated to pattern the vascular niche. This interplay model promoted physiologically relevant vascularized glandular morphogenesis and . We identified a reciprocal regulatory mechanism for promoting SGs regeneration via contact-independent cell communication and direct cell-cell interactions between SGs and the vasculature. We envision the successful use of our approach for vascularized organ regeneration in the near future.
众所周知,血管系统的整合在组织或器官功能再生中是有效的。然而,对表皮附属器与其血管微环境之间相互作用的模糊理解是获取汗腺(SG)特异性血管单元的首要障碍。在这里,我们绘制了它们精确的解剖连接,并报告SG细胞(SGC)与周围血管微环境之间的相互作用是腺体发育和内稳态维持的关键。为了复制这种相互作用,我们使用三维(3D)生物打印从分化的脂肪来源间充质干细胞(ADSC)生成可重复的SGC球体。与真皮微血管内皮细胞(DMEC)一起,由聚(ε-己内酯)(PCL)制成的牺牲模板被制造出来以构建血管微环境。这种相互作用模型促进了生理相关的血管化腺体形态发生。我们确定了一种通过接触非依赖性细胞通讯以及SG与血管系统之间的直接细胞-细胞相互作用来促进SG再生的相互调节机制。我们设想在不久的将来成功地将我们的方法用于血管化器官再生。