Key Laboratory of Animal Genetics, Breeding and Reproduction of Shaanxi Province, Laboratory of Animal Fat Deposition and Muscle Development, College of Animal Science and Technology, Northwest A & F University, Yangling, Shaanxi, China.
J Cell Physiol. 2020 Oct;235(10):7484-7495. doi: 10.1002/jcp.29652. Epub 2020 May 9.
miRNAs, a kind of noncoding small RNA, play a significant role in adipose differentiation. In this study, we explored the effect of miR-324-5p in adipose differentiation, and found that miR-324-5p could promote adipocytes differentiation and increase body weight in mice. We overexpressed miR-324-5p during adipocytes differentiation, by oil red O and bodipy staining found that lipid accumulation was increased, and the expression level of adipogenic related genes were significantly increased. And the opposite experimental results were obtained after inhibiting miR-324-5p. In vivo, we injected miR-324-5p agomiR in obese mice and found that body weight, adipocyte area, and adipogenic-related gene expression level were significantly increased but lipolytic genes were decreased. To further explore the mechanism of miR-324-5p regulation in lipid accumulation, we constructed Krueppel-like factor 3 (KLF3) 3'-untranslated region luciferase reporter vector and KLF3 pcDNA 3.1 overexpression vector, and found that miR-324-5p was able to directly target KLF3. Overall, in this study we found that miR-324-5p could promote mice preadipoytes differentiation and increase mice fat accumulation by targeting KLF3.
miRNAs 是一种非编码小分子 RNA,在脂肪分化中发挥重要作用。在本研究中,我们探讨了 miR-324-5p 在脂肪分化中的作用,发现 miR-324-5p 可促进脂肪细胞分化并增加小鼠体重。我们在脂肪细胞分化过程中过表达 miR-324-5p,通过油红 O 和 bodipy 染色发现脂质积累增加,脂肪生成相关基因的表达水平显著升高。而抑制 miR-324-5p 则得到了相反的实验结果。在体内,我们向肥胖小鼠注射 miR-324-5p agomiR,发现体重、脂肪细胞面积和脂肪生成相关基因表达水平显著增加,但脂肪分解基因减少。为了进一步探讨 miR-324-5p 调节脂质积累的机制,我们构建了 Krueppel 样因子 3(KLF3)3'-非翻译区荧光素酶报告载体和 KLF3 pcDNA3.1 过表达载体,并发现 miR-324-5p 能够直接靶向 KLF3。总之,在本研究中我们发现 miR-324-5p 可以通过靶向 KLF3 促进小鼠前脂肪细胞分化并增加小鼠脂肪积累。