通过微阵列和miRNA研究分析人胚胎干细胞治疗ii型糖尿病的调控途径。

IF 1.5 Q4 CELL BIOLOGY
American journal of stem cells Pub Date : 2018-06-01 eCollection Date: 2018-01-01
Geeta Shroff, Rhea Shroff, Rakesh Gupta
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引用次数: 0

摘要

糖尿病的发生是由于自身免疫对β细胞的破坏(1型)或对胰岛素作用的抵抗(2型)。多种常规药物用于治疗糖尿病,糖尿病与肾功能衰竭、失明和中风等长期并发症有关。我们最近在95例2型糖尿病患者中展示了人类胚胎干细胞(hESCs)的潜力。在本研究中,我们使用微阵列和miRNA研究来证明hESCs对糖尿病有效的原因。培养3个hESCs样本,采用微阵列技术分析糖尿病通路。利用基因本体(GO)和DAVID数据库分析miRNA的基因靶点。根据氧化石墨烯分析对参与糖尿病通路的基因进行分类。使用Reactome和Panther数据库确定这些基因的通路。所有相关基因的上调和下调均得到了显著p值的证实。胰岛素分泌、结合及其正向调控通路上调,而胰岛素负向调控通路显著下调。在我们的设施中培养的hESCs在移植后具有再生胰腺β细胞的能力;胰岛素分泌途径明显上调。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Analysis of the regulation pathways via microarray and miRNA studies: human embryonic stem cells to treat diabetes mellitus type-II.

Analysis of the regulation pathways via microarray and miRNA studies: human embryonic stem cells to treat diabetes mellitus type-II.

Diabetes mellitus occurs either due to an autoimmune destruction of β cells (Type 1) or resistance to insulin effects (Type 2). Diverse conventional medications are used for treatment of diabetes, which is associated with long term complications such as kidney failure, blindness, and stroke. We recently showed the potential of human embryonic stem cells (hESCs) in 95 patients with type 2 diabetes. In the present study, we use the microarray and miRNA studies to prove why hESCs are effective in diabetes. Three samples of hESCs were cultured and microarray technology was used for the analysis of diabetic pathways. The gene targets for miRNA were analyzed using gene ontology (GO) and DAVID database. Genes involved in the diabetic pathways were classified in accordance with GO analysis. Pathways for these genes were determined using Reactome and Panther databases. The up and down-regulation of all the genes involved were confirmed with the significant p-values. Pathways for insulin secretion, binding and its positive regulation were up-regulated while the pathways for negative regulation of insulin were significantly down-regulated. hESCs cultured at our facility have the capability to regenerate the pancreatic β cells after transplantation; as the insulin secretion pathways were significantly up-regulated.

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