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沉默信息调节因子1（SIRT1）基因敲低可增强人胚胎干细胞向胰腺β细胞的分化。

SIRT1 Knockdown Enhances the Differentiation of Human Embryonic Stem Cells into Pancreatic β Cells.

作者信息

Seo Nan-Hee, Song Hwa-Ryung, Han Myung-Kwan

机构信息

Dept. of Microbiology, Jeonbuk National University Medical School, Jeonju 54896, Korea.

出版信息

Dev Reprod. 2019 Dec;23(4):391-399. doi: 10.12717/DR.2019.23.4.391. Epub 2019 Dec 31.

DOI:10.12717/DR.2019.23.4.391
PMID:31993545
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6985299/
Abstract

Nicotinamide is used to maturate pancreatic progenitors from embryonic stem cells (ESCs) into insulin-producing cells (IPCs). It has been known that nicotinamide inhibits the enzymatic activity of SIRT1, an NAD-dependent deacetylase. Here we show that SIRT1 knockdown enhances the differentiation of human ESCs into IPCs. SIRT1 knockdown enhances the clustering size of IPCs and the expression of pancreatic genes including c-peptide, pancreas/duodenum homeobox protein 1 (PDX1), insulin, somatostatin, glucagon and Nkx6.1 in human ESC-derived IPCs. In addition, We found that IPCs differentiated from SIRT1 knockdowned human ESCs have more zinc compared to those from control human ESCs. Our data suggest that SIRT1 negatively regulates the differentiation of β cells from human ESCs.

摘要

烟酰胺被用于将胚胎干细胞（ESC）中的胰腺祖细胞诱导分化为胰岛素分泌细胞（IPC）。已知烟酰胺可抑制SIRT1（一种烟酰胺腺嘌呤二核苷酸依赖性脱乙酰酶）的酶活性。在此我们表明，敲低SIRT1可增强人类胚胎干细胞向胰岛素分泌细胞的分化。敲低SIRT1可增加人类胚胎干细胞来源的胰岛素分泌细胞的聚集大小，并增强包括C肽、胰腺/十二指肠同源盒蛋白1（PDX1）、胰岛素、生长抑素、胰高血糖素和Nkx6.1在内的胰腺基因的表达。此外，我们发现，与对照人类胚胎干细胞来源的胰岛素分泌细胞相比，敲低SIRT1的人类胚胎干细胞分化而来的胰岛素分泌细胞含有更多的锌。我们的数据表明，SIRT1对人类胚胎干细胞向β细胞的分化起负调控作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99c9/6985299/20c95a13a6e9/dr-23-4-391-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99c9/6985299/cd5080a23671/dr-23-4-391-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99c9/6985299/377021ab01d1/dr-23-4-391-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99c9/6985299/68879f24c96b/dr-23-4-391-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99c9/6985299/7e0497ba77ac/dr-23-4-391-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99c9/6985299/20c95a13a6e9/dr-23-4-391-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99c9/6985299/cd5080a23671/dr-23-4-391-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99c9/6985299/377021ab01d1/dr-23-4-391-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99c9/6985299/68879f24c96b/dr-23-4-391-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99c9/6985299/7e0497ba77ac/dr-23-4-391-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99c9/6985299/20c95a13a6e9/dr-23-4-391-g5.jpg

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