Identification of key genes and pathways associated with osteogenic differentiation of adipose stem cells

脂肪生成 Wnt信号通路 脂肪组织 生物 细胞生物学 间充质干细胞 细胞外基质 干细胞 基因调控网络 细胞分化 基因 基因表达 计算生物学 信号转导 遗传学 内分泌学
作者
Xinyuan Zhao,Minlu Liang,Xiaona Li,Xiaoling Qiu,Li Cui
出处
期刊:Journal of Cellular Physiology [Wiley]
卷期号:233 (12): 9777-9785 被引量:18
标识
DOI:10.1002/jcp.26943
摘要

Adipose stem cells (ASCs) are considered a great alternative source of mesenchymal stem cells (MSCs) and have shown great promise on tissue engineering and regenerative medicine applications, including bone repair. However, the underlying mechanisms regulating the osteogenic differentiation of ASCs remain poorly known. Gene expression profiles of GSE63754 and GSE37329 were downloaded from gene expression omnibus database. R software and Bioconductor packages were used to compare and identify the differentially expressed genes (DEGs) before and after ASC osteogenic differentiation. The common significant DEGs between GSE63754 and GSE37329 were then subjected to gene ontology (GO) enrichment analysis, ingenuity pathway analysis (IPA), and protein-protein interactions (PPIs) networks analysis. One of the central node genes FOXO1 was selected for further investigation. A total of 142 up- and 69 downregulated genes were aberrantly expressed in both GSE63754 and GSE37329. GO analysis revealed that these DEGs were associated with extracellular matrix organization, proteinaceous extracellular matrix, and Wnt-protein binding. IPA analysis showed that canonical pathways, such as FXR/RXR activation, adipogenesis pathway, and LXR/RXR activation, were involved in regulating osteogenic differentiation of ASCs. A total of three subnetworks and 39 nodes were identified with PPI network and MCODE plugin. Moreover, suppression of one central node gene FOXO1 inhibited the osteogenic differentiation of ASCs. Our study provides a registry of genes and pathways that play important roles in regulating osteogenic differentiation of ASCs, which might have potential therapeutic applications in bone regeneration and bone tissue engineering.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
1秒前
大模型应助ysh采纳,获得10
2秒前
东方元语应助勤劳翰采纳,获得20
4秒前
4秒前
深情安青应助维E真采纳,获得10
4秒前
zuzu应助维E真采纳,获得10
4秒前
FashionBoy应助维E真采纳,获得10
4秒前
斯文败类应助维E真采纳,获得10
5秒前
奔跑应助维E真采纳,获得10
5秒前
彭于晏应助维E真采纳,获得10
5秒前
科研通AI6.2应助乘风采纳,获得10
6秒前
香蕉觅云应助jinzhen采纳,获得10
8秒前
9秒前
10秒前
10秒前
lzzzz发布了新的文献求助10
11秒前
ICY完成签到,获得积分10
11秒前
12秒前
Akim应助蔡宇滔采纳,获得10
13秒前
高大代容发布了新的文献求助10
15秒前
赘婿应助执着的过客采纳,获得10
15秒前
hongxing liu完成签到,获得积分10
15秒前
毗昙发布了新的文献求助10
15秒前
15秒前
16秒前
大个应助贾硕士采纳,获得10
16秒前
顾矜应助张淑涵采纳,获得10
17秒前
ysh发布了新的文献求助10
17秒前
18秒前
独特的映菱完成签到,获得积分10
18秒前
CodeCraft应助XFF采纳,获得10
19秒前
李洁完成签到,获得积分10
19秒前
jinzhen发布了新的文献求助10
20秒前
CipherSage应助Diego采纳,获得10
21秒前
酷波er应助Diego采纳,获得10
21秒前
leo_plj完成签到,获得积分10
22秒前
22秒前
22秒前
22秒前
23秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Reducing Compassion Fatigue, Secondary Traumatic Stress and Burnout 600
China Pluperfect I: Epistemology of Past and Outside in Chinese Art 520
Matrix Methods in Data Mining and Pattern Recognition Second Edition 510
Mammalian Synthetic Biology 500
Auslegungsgeschichte 500
Cosmos as Art Object: Studies in Plato's Timaeus and Other Dialogues 500
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 工程类 有机化学 化学工程 生物化学 计算机科学 内科学 物理 复合材料 催化作用 细胞生物学 无机化学 光电子学 物理化学 电极 基因
热门帖子
关注 科研通微信公众号,转发送积分 7638098
求助须知:如何正确求助?哪些是违规求助? 9211411
关于积分的说明 19758652
捐赠科研通 7205015
什么是DOI,文献DOI怎么找? 3275778
关于科研通互助平台的介绍 2437385
邀请新用户注册赠送积分活动 2272954