Folic acid promotes proliferation and differentiation of porcine pancreatic stem cells into insulin-secreting cells through canonical Wnt and ERK signaling pathway

Wnt信号通路 胰岛素 MAPK/ERK通路 细胞生长 细胞生物学 生物 干细胞 细胞分化 胰岛素受体 信号转导 化学 内分泌学 胰岛素抵抗 生物化学 基因
作者
Hong Yang,Dezhe Qin,Shuanshuan Xu,Chen He,Jing Sun,Jinlian Hua,Sha Peng
出处
期刊:The Journal of Steroid Biochemistry and Molecular Biology [Elsevier BV]
卷期号:205: 105772-105772 被引量:13
标识
DOI:10.1016/j.jsbmb.2020.105772
摘要

• Folic acid promotes the proliferation of pPSCs by binding to FOLRα. • Folic acid increases the efficiency of directed differentiation of pPSCs into insulin-producing cells in vitro . • Canonical Wnt and ERK signaling pathway participate in the regulation of folic acid on proliferation and differentiation of pPSCs. Porcine pancreatic stem cells (pPSCs) can be induced to differentiate into insulin-producing cells in vitro and thus serve as a major cells source for β-cell regeneration. However, this application is limited by the weak cell proliferation ability and low insulin induction efficiency. In this study, we explored the role of folic acid in the proliferation of pPSCs and the formation of insulin-secreting cells. We found that FA-treated pPSCs cells had a high EDU positive rate, and the proliferation marker molecules PCNA, CyclinD1 and c-Myc were up-regulated, while the expression of folate receptor α (FOLRα) was up-regulated. In further research, interference FOLRα or adding canonical Wnt signaling pathway or ERK signaling pathway inhibitors could significantly inhibit the effect of FA on pPSCs proliferation. Meanwhile, during the differentiation of pPSCs into insulin-secreting cells, we found that the maturation marker genes Insulin, NKX6.1, MafA, and NeuroD1 was upregulated in insulin-secreting cell masses differentiationed from pPSCs after FA treatment, and the functional molecules Insulin and C-peptide were increased, the ability to secrete insulin in response to high glucose was also increased. With the addition of Wnt and ERK signaling pathway inhibitors, the pro-differentiation effect of FA was weakened. In conclusion, FA promotes the proliferation of pPSCs by binding to folate receptor α (FOLRα) and increase the efficiency of directed differentiation of pPSCs into insulin-producing cells by regulating canonical Wnt and ERK signaling pathway. This study lays theoretical foundation for solving the bottleneck in the treatment of diabetes with stem cell transplantation in future.
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