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运动训练驱动的外体miRNA-323-5p活性通过DUSP3/ERK通路抑制3T3-L1细胞的脂肪转化

Seita Osawa¹, Hisashi Kato², Daigo Kemmoku³

¹Graduate School of Health and Sports Science, Doshisha University, 1-3 Tatara-Miyakodani, Kyotanabe City, Kyoto, 610-0394, Japan; Japan Society for the Promotion of Sci., Tokyo, Japan.

Biochemical and biophysical research communications

|July 31, 2024

概括

经过运动训练的老鼠外生体 (EX-ASCexos) 抑制脂肪细胞 (脂肪细胞) 的分化. 这种效应是由外体微RNA-323-5p (miR-323-5p) 介导的,它会影响像PPARγ这样的关键脂肪生成蛋白.

科学领域:

生物化学生物化学
细胞生物学细胞生物学
分子生物学分子生物学

背景情况:

脂肪源干细胞 (ASC) 释放的外体细胞 (ASCexos) 具有不同的生物功能.
运动会影响新陈代谢过程,可能是通过诸如外体的分泌因子.

研究的目的:

研究运动训练老鼠 (EX-ASCexos) 的外体对3T3-L1细胞脂肪基分化的影响.
在EX-ASCexos中识别特定的microRNAs (miRNAs),负责观察到的效应.

主要方法:

3T3-L1细胞通过使用EX-ASCexos或静止大鼠 (SED-ASCexos) 的外体分化为脂肪细胞.
分析了与脂肪生成相关的蛋白质和miRNA表达.
特定的外体miRNAs被确定并使用模仿器进行功能测试.

主要成果:

EX-ASCexos,但不是SED-ASCexos,减弱的3T3-L1脂肪细胞分化.
这种抑制与非活性PPARγ (-Ser112PPARγ) 的增加,-Thr202/Tyr204ERK的升高和DUSP3.3的降低相关.
miR-323-5p,miR-433-3p和miR-874-3p都在EX-ASCexos中进行了丰富.
miR-323-5p模仿复制了对脂肪生成的抑制作用.

结论:

运动训练衍生的外体miR-323-5p抑制3T3-L1脂肪生成.
该机制涉及增加不活跃的PPARγ,并通过ERK信号抑制DUSP3.

关键词:

增脂生殖是一种增脂的过程.脂肪组织衍生干细胞的干细胞.具有双重特异性的酸酶3 外基因组是外基因组中的一个.细胞外信号调节的激酶.这是一个小RNARNA.

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