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首页> 外文期刊>Journal of Cellular Physiology >Acyl‐CoA synthetase short‐chain family member 2 (ACSS2) is regulated by SREBP‐1 and plays a role in fatty acid synthesis in caprine mammary epithelial cells
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Acyl‐CoA synthetase short‐chain family member 2 (ACSS2) is regulated by SREBP‐1 and plays a role in fatty acid synthesis in caprine mammary epithelial cells

机译：酰基激酶短链家庭成员应承担的2(ACSS2)监管,如1和发挥作用在山羊的乳脂肪酸合成上皮细胞

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摘要

Sterol regulatory element binding protein 1 (SREBP‐1) is well‐known as the master regulator of lipogenesis in rodents. Acyl‐CoA synthetase short‐chain family member 2 (ACSS2) plays a key role in lipogenesis by synthesizing acetyl‐CoA from acetate for lipogenesis. ATP citrate lyase (ACLY) catalyzes the conversion of citrate and coenzyme A to acetyl‐CoA, hence, it is also important for lipogenesis. Although ACSS2 function in cancer cells has been elucidated, its essentiality in ruminant mammary lipogenesis is unknown. Furthermore, ACSS2 gene promoter and its regulatory mechanisms have not known. Expression of ACSS2 was high in lipid synthesizing tissues, and its expression increased during lactation compared with non‐lactating period. Simultaneous knockdown of both ACSS2 and ACLY by siRNA in primary goat mammary epithelial cells decreased ( p ??0.05) the mRNA abundance of genes associated with de novo fatty acid synthesis ( FASN , ACACA , SCD1 ) and triacylglycerol (TAG) synthesis ( DGAT1 , DGAT2 , GPAM , and AGPAT6 ). Genes responsible for lipid droplet formation and secretion ( PLIN2 and PLIN3 ) and fatty acid oxidation ( ATGL , HSL , ACOX , and CPT1A ) all decreased ( p ??0.05) after ACSS2 and ACLY knockdown. Total cellular TAG content and lipid droplet formation also decreased. Use of a luciferase reporter assay revealed a direct regulation of ACSS2 by SREBP‐1. Furthermore, SREBP‐1 interacted with an SRE (SREBP response element) spanning at ?475 to ?483?bp on the ACSS2 promoter. Taken together, our results revealed a novel pathway that SREBP‐1 may regulate fatty acid and TAG synthesis by regulating the expression of ACSS2 .
机译：固醇调节元件结合蛋白1(如1)应承担的量称为主监管机构啮齿动物的脂肪生成。短链应承担家庭成员2 (ACSS2)扮演了一个关键在脂肪生成作用,合成乙酰辅酶a来自于脂肪生成醋酸。柠檬酸(ac)催化的转换辅酶A地理乙酰辅酶A,因此,它也是重要的脂肪生成。函数在癌细胞已经阐明,其重要性在反刍动物乳腺脂肪生成未知的。监管机制不清楚。ACSS2是高脂质合成组织,哺乳期间及其表达增加相比之下,非哺乳期里。可拆卸的siRNA ACSS2和交流主要山羊乳腺上皮细胞减少(0.05 p & ?)基因的mRNA丰富与新创脂肪酸合成相关(FASN ACACA SCD1) and triacylglycerol(一天)一个综合体。(DGAT1 DGAT2、GPAM和AGPAT6)。负责脂滴的形成和基因分泌(PLIN2和PLIN3)和脂肪酸氧化(ATGL奥软、ACOX CPT1A)减少(p & ? 0.05) ACSS2和交流之后可拆卸的。液滴的形成也降低了。荧光素酶报告实验显示直接ACSS2监管,如1所示。如1互动与行为(如反应元素)跨越? 475 ? 483 ?启动子。新途径,如5月1日调节脂肪酸和标记合成通过调节ACSS2的表情。

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