| Summary: | 碩士 === 國防醫學院 === 生物及解剖學研究所 === 101 === The organogenesis of tooth starts with the thickening of oral epithelium. Subsequent to the increase in thickness, oral epithelial cells initiate the reciprocal signaling with the underlying ectomesenchyme. The epithelial cells differentiate into ameloblasts to form enamel while the ectomesenchymal cells differentiate into other cells to form the remaining tooth structures. However, the regeneration of enamel is still not feasible because the enamel epithelium is degenerated once the enamel formation is completed and leaves no ameloblasts in situ for further manipulation. Also the whole tooth regeneration is not possible without the embryonic epithelium to initiate the reciprocal signaling activities.
In 2006, the discovery of genomic reprogramming of human somatic cells to embryonic stem cells (ESCs)-like pluripotent state provides a unique opportunity for stem cell research. The reprogrammed cells, named as induced pluripotent stem cells (iPSCs), possess many similar properties as ESCs while keep the original cells’ characteristics. Therefore, it is expected that dental cell-derived iPSCs own higher potential than others in regenerating tooth structures. In this study, we are going to create iPSCs from human dental pulp cells first. Created iPSCs will be induced into an ectoderm cell lineage and then cocultured with dental stem cells of mesenchymal origin. The goal is to recreate the reciprocal signaling events happening between original dental epithelium and mesenchyme to successfully regenerate a complete tooth.
On the other hand, iPSCs create the personal cell origin. We can use iPSCs to investigate human diseases which lack of experimental animal platforms. Thus, we can study of drug screening and development, and create the personalized medical platform. In this study, we were going to investigate Best disease. We obtained the patient’s dental pulp cells, reprogrammed into iPSCs (Best-iPSCs), and compared with the iPSCs from normal person. In Best-iPSCS, these two proteins: Bestrophin-1 and STXBP2, had expression levels significantly lower than non-diseased iPSCs. In the future, we are going to further investigate this phenomenon and their correlation with the Best disease.
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