近日,，中科院廣州生物醫(yī)藥與健康研究院裴端卿博士領(lǐng)導(dǎo)的研究團(tuán)隊(duì)通過(guò)人鼠組織重組的培養(yǎng)體系證實(shí)了人尿液多能干細(xì)胞可被用于構(gòu)建再生牙齒,。這是科學(xué)家首次利用人誘導(dǎo)多能干細(xì)胞獲得成型的再生器官。該研究成果于7月30日在線發(fā)表在學(xué)術(shù)期刊Cell Regeneration上,。
由于牙源性上皮細(xì)胞在成體中已無(wú)法獲得,，裴端卿研究團(tuán)隊(duì)通過(guò)誘導(dǎo)尿液細(xì)胞來(lái)源的多能干細(xì)胞分化為上皮樣的膜狀結(jié)構(gòu)，取代再生牙齒的構(gòu)建必須得上皮組織,。該誘導(dǎo)多能干細(xì)胞衍生的上皮組織接受小鼠牙胚間充質(zhì)的成牙信號(hào),，共同啟動(dòng)了再生牙齒的發(fā)生發(fā)育，并在移植到免疫缺陷鼠體內(nèi)3周后形成了牙樣結(jié)構(gòu),。這些牙樣結(jié)構(gòu)具有人牙齒的正常結(jié)構(gòu),，其中成釉細(xì)胞和牙釉質(zhì)是由尿液誘導(dǎo)多能干細(xì)胞衍生的上皮組織發(fā)育而來(lái)的。此外,，這些牙樣結(jié)構(gòu)與正常人牙有相似的理化性質(zhì),，包括相似的硬度、彈性模量和一致的化學(xué)組成成分,。
雖然該牙齒再生方法中還存在一些問(wèn)題,，如小鼠細(xì)胞的參與、30％的成牙率以及釉質(zhì)硬度較低等,，但未來(lái)可以通過(guò)人源間充質(zhì)細(xì)胞的取代和培養(yǎng)體系的優(yōu)化解決克服這些不足,。該研究成果將為今后實(shí)現(xiàn)再生牙齒臨床個(gè)性化治療奠定重要基礎(chǔ)。（生物谷 Bioon.com）
生物谷推薦的英文摘要
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.
