To Investigate the Potential Application of Mesenchymal Stem Cellsfrom Human Umbilical Cord to Treat Type 1 DM by TransducingTranscription Factors of β-cell

• Main Authors: Wei, Meichun, 魏梅君
• Other Authors: Chan, Yihsin
• Format: Others
• Language: zh-TW
• Published: 2011
• Online Access: http://ndltd.ncl.edu.tw/handle/50973101458759141569

碩士 === 國防醫學院 === 微生物及免疫學研究所 === 99 === Type 1 diabetes is an autoimmune disease. The main reason to develop this disease is the patients’ beta cells attacked by their own immune systems and result in the beta cells producing little or no insulin and making patients with hyperglycemia. Pancreas transplantation is the most effective therapy for type 1 diabetes, but there are just a few patients who could be donated. However, most people with type 1 diabetes must take daily injections of insulin due to dysfunction of β-cell. Therefore, trying to find new sources for treating type 1 diabetes instead of pancreas transplantation is developing and one of the most attractive researches is using stem cell as cell therapy. There are many studies to focus on stem cells for curing diabetes. The investigators used the stem cells from pancreatic ducts, livers, guts or bone marrow. However, the sources are still limited and the application is restricted. Recent studies have pointed out that mesenchymal stem cells (MSCs) isolates from human umbilical cord, namely Wharton’ s jelly, are easily acquired and useful. They are multipotent stem cells and have been shown to differentiate into various lineages. In this project, we used three kinds of transcription factors during β-cell development to differentiate mesenchymal stem cells into β-cell. These transcription factors are crucial for β-cell differentiation, including PDX-1 (Pancreatic and duodenal homeobox 1), Ngn3 (neurogenin3), and MafA (v-maf musculoaponeurotic fibrosarcoma oncogene homolog A). In the previous study, we have confirmed PDX1+ MSCs could control the blood glucose in diabetic rats. In this study, we used these three transcription factors to regulate MSCs differentiating into insulin-secreting cells by lentiviral transduction. The results showed these mesenchymal stem cells could differentiate into insulin-producing cells. We will use NOD mice as the animal model to investigate the effect of these insulin-producing cells. We hope this approach will create a new therapy for type 1 diabetes.