Sox6 impairs the adipogenic commitment of mesenchymal stem cells by targeting lysyl oxidase and preadipocyte factor 1

脂肪生成 间充质干细胞 细胞生物学 转录因子 脂肪组织 生物 赖氨酰氧化酶 HDAC1型 组蛋白脱乙酰基酶 内分泌学 组蛋白 生物化学 基因 细胞外基质
作者
Shao-yue Du,Hu L,Bing-He Zhou,Ze Zhang,Mingchao Li,Dong Chang,Cong-Jian Xu,Xin Dou
出处
期刊:Biochemical and Biophysical Research Communications [Elsevier BV]
卷期号:681: 225-231 被引量:2
标识
DOI:10.1016/j.bbrc.2023.09.084
摘要

The commitment of mesenchymal stem cells (MSCs) to preadipocytes and the termination of differentiation to adipocytes are critical for maintaining systemic energy homeostasis. However, our knowledge of the molecular mechanisms governing the commitment of MSCs to preadipocytes and the subsequent termination of their differentiation into adipocytes remain limited. Additionally, the role of Sox6 sex-determining region Y (SRY)-box6 (Sox6), a transcription factor that regulates gene transcription, is reportedly involved in various cellular processes, including adipogenesis; however, its function in regulating preadipocyte development and the factors involved in the termination of adipogenic differentiation remain unexplored. Therefore, we investigated the role of Sox6 in regulating the differentiation of adipocytes by monitoring the effects of its overexpression in C3H10T1/2 cells (in vitro) and C57BL/6J mouse (in vivo) models of adipogenesis. We observed lower Sox6 expression in the adipose tissue of obese mice than that in control mice. Sox6 overexpression inhibited the differentiation of MSC by directly binding to the lysyl oxidase (Lox) and preadipocyte factor 1 (Pref1) promoters, which was potentiated by histone deacetylase-1(HDAC1). Our findings suggest that Sox6 is a key regulator of MSC commitment to adipocytes; therefore, targeting the Sox6-mediated regulation of this process could offer potential therapeutic avenues for addressing obesity and related metabolic disorders.
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
林风眠完成签到,获得积分10
刚刚
Clover04发布了新的文献求助20
刚刚
浮尘完成签到,获得积分10
1秒前
WYang完成签到,获得积分10
1秒前
niubi666完成签到,获得积分10
1秒前
内向南风完成签到 ,获得积分10
1秒前
月月完成签到,获得积分10
2秒前
soufle完成签到,获得积分10
3秒前
luozejun完成签到,获得积分10
3秒前
斯文的碧完成签到,获得积分10
3秒前
崔正成完成签到,获得积分10
4秒前
顾矜的应助被洁净糖豆采纳,获得10
4秒前
5秒前
5秒前
Yvonne完成签到,获得积分10
6秒前
我爱看文献完成签到,获得积分10
6秒前
Abel完成签到 ,获得积分10
6秒前
檀俊杰完成签到,获得积分10
7秒前
阿明完成签到 ,获得积分10
7秒前
科目三的应助被杜晓倩采纳,获得10
7秒前
先字母完成签到,获得积分10
8秒前
8秒前
阿白完成签到,获得积分10
8秒前
2233完成签到 ,获得积分10
9秒前
清欢渡完成签到 ,获得积分10
9秒前
xiaoxiao完成签到,获得积分10
10秒前
Leo的应助被JasonMen采纳,获得10
10秒前
科研通AI6.4的应助被HXZ采纳,获得200
10秒前
不吃香菜完成签到,获得积分10
10秒前
10秒前
江水边发布了新的文献求助10
10秒前
juner1111完成签到,获得积分10
11秒前
ashore完成签到,获得积分10
11秒前
11秒前
专注智宸发布了新的文献求助10
11秒前
聪明的小梁完成签到,获得积分10
12秒前
Haibrar发布了新的文献求助10
12秒前
12秒前
好多好多鱼完成签到,获得积分10
12秒前
Li_wang完成签到,获得积分10
12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
Aspects of Post-SPE Phonology 2000
CODESSA Version 2.13 for Windows 2000
Rosenblum, Global Change Biology 800
Berberine regulates the TLR4 signaling pathway to suppress hypoxia-induced proliferation and migration of pulmonary arterial smooth muscle cells 520
Organizational Behavior 510
A Concise Course in Continuum Mechanics 400
热门求助领域 (近24小时)
化学 材料科学 医学 生物 计算机科学 工程类 纳米技术 有机化学 化学工程 内科学 物理 生物化学 复合材料 催化作用 细胞生物学 人工智能 心理学 无机化学 基因 遗传学
热门帖子
关注 科研通微信公众号,转发送积分 7847258
求助须知:如何正确求助?哪些是违规求助? 9367329
关于积分的说明 20654986
捐赠科研通 7444056
什么是DOI,文献DOI怎么找? 3342024
关于科研通互助平台的介绍 2485919
邀请新用户注册赠送积分活动 2364930