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微小RNA-26a通过调控ACADM和ACSL1基因以及细胞周期进程抑制猪脂肪生成。

MiR-26a Inhibits Porcine Adipogenesis by Regulating ACADM and ACSL1 Genes and Cell Cycle Progression.

作者信息

Zhang Dongjie, Hao Wanjun, Zhu Rongru, Wang Liang, Wu Xiaoxu, Tian Ming, Liu Di, Yang Xiuqin

机构信息

Institute of Animal Husbandry, Heilongjiang Academy of Agricultural Sciences, Harbin 150086, China.

College of Animal Science and Technology, Northeast Agricultural University, Harbin 150030, China.

出版信息

Animals (Basel). 2024 Dec 3;14(23):3491. doi: 10.3390/ani14233491.

DOI:10.3390/ani14233491
PMID:39682455
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11640176/
Abstract

MicroRNAs play essential roles in biological processes by regulating gene expression at the post-transcriptional level. Our previous studies suggested the role of miR-26a in porcine fat accumulation. Here, through gain- and loss-of-function analyses, we first showed that miR-26a increased the proliferation of porcine preadipocytes by promoting cell division and that miR-26a inhibited the preadipocyte differentiation. Next, acyl-CoA dehydrogenase, medium chain (ACADM) was revealed to promote the proliferation and differentiation of preadipocytes for the first time. Then, it was revealed that miR-26a regulates adipogenesis by directly binding to the 3' untranslated region of ACADM and the long-chain acyl-Co A synthetase 1 (ACSL1) gene, a previously known regulator of adipogenesis. Finally, RNA-sequencing, performed on preadipocytes overexpressing miR-26a, identified 337 differentially expressed genes in the early stage of adipogenesis; among them, nine genes were characterized as potential targets of miR-26a. The 337 genes were mainly involved in Gene Ontology terms related to cell division, indicating that cell cycle progression was also a major event regulated by miR-26a during adipogenesis. We provide novel data for understanding the molecular mechanisms underlying adipogenesis, which will contribute to controlling fat accumulation in animals.

摘要

微小RNA通过在转录后水平调节基因表达在生物过程中发挥重要作用。我们之前的研究表明miR-26a在猪脂肪积累中发挥作用。在此,通过功能获得和功能缺失分析,我们首先表明miR-26a通过促进细胞分裂增加猪前体脂肪细胞的增殖,并且miR-26a抑制前体脂肪细胞分化。接下来,首次揭示中链酰基辅酶A脱氢酶(ACADM)促进前体脂肪细胞的增殖和分化。然后,揭示miR-26a通过直接结合ACADM的3'非翻译区和长链酰基辅酶A合成酶1(ACSL1)基因(一种先前已知的脂肪生成调节因子)来调节脂肪生成。最后,对过表达miR-26a的前体脂肪细胞进行RNA测序,在脂肪生成早期鉴定出337个差异表达基因;其中,9个基因被鉴定为miR-26a的潜在靶标。这337个基因主要参与与细胞分裂相关的基因本体论术语,表明细胞周期进程也是miR-26a在脂肪生成过程中调节的主要事件。我们提供了新的数据来理解脂肪生成的分子机制,这将有助于控制动物的脂肪积累。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9948/11640176/0d74251545e9/animals-14-03491-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9948/11640176/246914b7645d/animals-14-03491-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9948/11640176/8729d55201ac/animals-14-03491-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9948/11640176/3d41c84d9944/animals-14-03491-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9948/11640176/27d1c9f7e83a/animals-14-03491-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9948/11640176/85878900a45c/animals-14-03491-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9948/11640176/0d74251545e9/animals-14-03491-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9948/11640176/246914b7645d/animals-14-03491-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9948/11640176/8729d55201ac/animals-14-03491-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9948/11640176/3d41c84d9944/animals-14-03491-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9948/11640176/27d1c9f7e83a/animals-14-03491-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9948/11640176/85878900a45c/animals-14-03491-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9948/11640176/0d74251545e9/animals-14-03491-g006.jpg

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