近日，中科院广州生物医药与健康研究院裴端卿博士领导的研究团队通过人鼠组织重组的培养体系证实了人尿液多能干细胞可被用于构建再生牙齿。这是科学家首次利用人诱导多能干细胞获得成型的再生器官。该研究成果于7月30日在线发表在学术期刊Cell Regeneration上。
由于牙源性上皮细胞在成体中已无法获得，裴端卿研究团队通过诱导尿液细胞来源的多能干细胞分化为上皮样的膜状结构，取代再生牙齿的构建必须得上皮组织。该诱导多能干细胞衍生的上皮组织接受小鼠牙胚间充质的成牙信号，共同启动了再生牙齿的发生发育，并在移植到免疫缺陷鼠体内3周后形成了牙样结构。这些牙样结构具有人牙齿的正常结构，其中成釉细胞和牙釉质是由尿液诱导多能干细胞衍生的上皮组织发育而来的。此外，这些牙样结构与正常人牙有相似的理化性质，包括相似的硬度、弹性模量和一致的化学组成成分。
虽然该牙齿再生方法中还存在一些问题，如小鼠细胞的参与、30％的成牙率以及釉质硬度较低等，但未来可以通过人源间充质细胞的取代和培养体系的优化解决克服这些不足。该研究成果将为今后实现再生牙齿临床个性化治疗奠定重要基础。（生物谷 Bioon.com）
生物谷推荐的英文摘要
Cell Regeneration doi:10.1186/2045-9769-2-3
SNX16 negatively regulates the migration and tumorigenesis of MCF-7 cells
Leilei Zhang, Dajiang Qin, Chunfang Hao, Xiaodong Shu* and Duanqing Pei
Background
Sorting nexins are a large family of proteins that are associated with various components of the endosome system and they play many roles in processes such as endocytosis, intracellular protein trafficking and cell signaling. The subcellular distribution patterns of many of them remain controversial and their in vivo functions have not been characterized yet.
Results
We investigated the subcellular distribution and function of SNX16 in this study. SNX16 is detected on Rab5-positive endosomes localized adjacent to focal adhesions at cell cortex. Inhibition of SNX23, polymerization of microtubule filaments as well as the PI3-kinase all disrupt the cell cortex distribution of SNX16. Ectopic expression of SNX16 reduces the migration and the tumor formation activity of MCF-7 cells.
Conclusion
Our results indicate that, in addition to the PI3P, there is a SNX23- and microtubule-dependent cargo transport pathway required for the proper subcellular distribution of SNX16. SNX16 plays a negative regulatory role during cell migration and tumorigenesis.
