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miR-29a调节硬脂酰辅酶A去饱和酶(SCD)的表达,并在幼年遗传改良养殖罗非鱼中对饱和脂肪酸饮食作出反应而受到调控。

miR-29a modulates SCD expression and is regulated in response to a saturated fatty acid diet in juvenile genetically improved farmed tilapia ().

作者信息

Qiang Jun, Tao Yi Fan, He Jie, Sun Yi Lan, Xu Pao

机构信息

Key Laboratory of Freshwater Fisheries and Germplasm Resources Utilization, Ministry of Agriculture, Freshwater Fisheries Research Center, Chinese Academy of Fishery Sciences, Wuxi, Jiangsu 214081, China

Key Laboratory of Freshwater Fisheries and Germplasm Resources Utilization, Ministry of Agriculture, Freshwater Fisheries Research Center, Chinese Academy of Fishery Sciences, Wuxi, Jiangsu 214081, China.

出版信息

J Exp Biol. 2017 Apr 15;220(Pt 8):1481-1489. doi: 10.1242/jeb.151506. Epub 2017 Feb 6.

Abstract

MicroRNAs (miRNAs) are small non-coding RNAs that regulate target gene expression by binding to the 3' untranslated region (3' UTR) of the target mRNA. MiRNAs regulate a large variety of genes, including those involved in liver biology and disease. Here, we report for the first time that miR-29a post-transcriptionally regulates stearoyl-CoA desaturase (SCD) by binding to its 3' UTR in genetically improved farmed tilapia (GIFT), , as shown by a 3' UTR luciferase reporter assay. miR-29a antagomir treatment resulted in significant upregulation of SCD expression. We found that miR-29a expression was negatively correlated with SCD expression in GIFT liver. Inhibition of miR-29a led to a significant increase in SCD expression on day 60 induced by a saturated fatty acid diet, thereby increasing conversion of 16:0 and 18:0 to 16:1 and 18:1, respectively, and activating serum insulin, which would favor glucose and lipid uptake by the liver. These results indicate that miR-29a regulates SCD levels by binding to its 3' UTR, and this interaction affects saturated fatty acid stress induction and insulin and lipid accumulation in serum. Our results suggest that miR-29a is critical in regulating lipid metabolism homeostasis in GIFT liver, and this might provide a basis for understanding the biological processes and therapeutic intervention encountered in fatty liver.

摘要

微小RNA(miRNA)是一类小的非编码RNA,通过与靶mRNA的3'非翻译区(3'UTR)结合来调节靶基因的表达。miRNA调节多种基因,包括那些参与肝脏生物学和疾病的基因。在此,我们首次报道在遗传改良尼罗罗非鱼(GIFT)中,miR-29a通过与其3'UTR结合在转录后水平调节硬脂酰辅酶A去饱和酶(SCD),3'UTR荧光素酶报告基因检测证实了这一点。miR-29a拮抗剂处理导致SCD表达显著上调。我们发现GIFT肝脏中miR-29a的表达与SCD的表达呈负相关。抑制miR-29a导致在饱和脂肪酸饮食诱导的第60天SCD表达显著增加,从而分别增加16:0和18:0向16:1和18:1的转化,并激活血清胰岛素,这有利于肝脏对葡萄糖和脂质的摄取。这些结果表明,miR-29a通过与其3'UTR结合来调节SCD水平,这种相互作用影响饱和脂肪酸应激诱导以及血清中胰岛素和脂质的积累。我们的结果表明,miR-29a在调节GIFT肝脏脂质代谢稳态中起关键作用,这可能为理解脂肪肝中遇到的生物学过程和治疗干预提供基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c7c/5413068/91ee9558ef5a/jexbio-220-151506-g1.jpg

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