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miR-10a-3p通过TGF-β1/Smad3信号通路调节脂肪和抑制脂肪炎症

Sonia Kiran¹, Mousumi Mandal¹, Ahmed Rakib¹

¹Department of Pharmaceutical Sciences, College of Pharmacy, The University of Tennessee Health Science Center, Memphis, TN, United States.

Frontiers in immunology

|June 19, 2023

概括

微RNA-10a-3p模仿剂通过准TGF-β1/Smad3信号传递来减少脂肪炎症并改善代谢标志物. 这一发现为与肥胖相关的代谢障碍提供了一种新的治疗策略.

科学领域:

生物化学生化学
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

肥胖是一种复杂的疾病,其特点是过多的脂肪积累和脂肪组织 (AT) 慢性低度炎症.
在肥胖期间,微RNA (miRs) 在调节AT炎症和脂肪细胞分化方面发挥着至关重要的作用.
这项研究研究了miR-10a-3p在脂肪炎症和脂肪生成中的特定作用和机制.

研究的目的:

使用ex vivo和体外模型评估miR-10a-3p在脂肪炎症和脂肪生成中的作用和机制.
为了确定饮食诱导的肥胖小鼠AT免疫细胞内miR表达的变化.
确定miR-10a-3p调制对炎症通路和脂肪细胞功能的影响.

主要方法:

从正常 (ND) 和高脂肪饮食 (HFD) 的小鼠的脂肪组织免疫细胞中对miR表达的比较分析.
在体外机理学研究中使用了3T3-L1脂肪细胞.
采用miR-10a-3p的分子模仿物来评估其对炎症基因表达和脂质积累的影响.

主要成果:

微阵列分析揭示了HFD小鼠的AT免疫细胞中下调的miR-10a-3p表达.
miR-10a-3p模仿了减少的M1巨标记物,炎症性细胞因子 (TGF-β1,IL-17F) 和KLF4,同时增加了FoxP3.
在3T3-L1脂肪细胞中,miR-10a-3p通过抑制TGF-β1,Smad3,CHOP-10和FASN来模仿减少的促炎性基因表达和脂质积累.

结论:

miR-10a-3p模仿剂缓解脂肪炎症并改善代谢参数,可能通过TGF-β1 / Smad3信号通路.
这项研究强调miR-10a-3p作为脂肪炎症和相关代谢障碍的潜在治疗点.

关键词:

在TGF-β1中.脂肪细胞 (adipocytes) 是一种脂肪细胞.这是一种炎症炎症炎症炎症.这是一个微型RNA.肥胖肥胖肥胖肥胖肥胖肥胖肥胖肥胖

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