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Long noncoding RNA ZFP36L2-AS functions as a metabolic modulator to regulate muscle development

文献类型： 外文期刊

作者： Cai, Bolin 1 ; Ma, Manting 1 ; Zhang, Jing 1 ; Kong, Shaofen 1 ; Zhou, Zhen 1 ; Li, Zhenhui 1 ; Abdalla, Bahareldin Ali 1 ; Xu, Haiping 1 ; Zhang, Xiquan 1 ; Lawal, Raman Akinyanju 5 ; Nie, Qinghua 1 ;

作者机构： 1.South China Agr Univ, Coll Anim Sci, Lingnan Guangdong Lab Modern Agr, Guangzhou 510642, Guangdong, Peoples R China

2.South China Agr Univ, Coll Anim Sci, State Key Lab Conservat & Utilizat Subtrop Agrobi, Guangzhou 510642, Guangdong, Peoples R China

3.Minist Agr, Guangdong Prov Key Lab Agroanim Genom & Mol Breed, Guangzhou 510642, Guangdong, Peoples R China

4.Minist Agr, Key Lab Chicken Genet Breeding & Reprod, Guangzhou 510642, Guangdong, Peoples R China

5.Jackson Lab, 600 Main St, Bar Harbor, ME 04609 USA

期刊名称：CELL DEATH & DISEASE （ 影响因子：9.685； 五年影响因子：9.624 ）

ISSN： 2041-4889

年卷期： 2022 年 13 卷 4 期

页码：

收录情况： SCI

摘要： Skeletal muscle is the largest metabolic organ in the body, and its metabolic flexibility is essential for maintaining systemic energy homeostasis. Metabolic inflexibility in muscles is a dominant cause of various metabolic disorders, impeding muscle development. In our previous study, we found IncRNA ZFP36L2-AS (for "ZFP36L2-antisense transcript") is specifically enriched in skeletal muscle. Here, we report that ZFP36L2-AS is upregulated during myogenic differentiation, and highly expressed in breast and leg muscle. In vitro, ZFP36L2-AS inhibits myoblast proliferation but promotes myoblast differentiation. In vivo, ZFP36L2-AS facilitates intramuscular fat deposition, as well as activates fast-twitch muscle phenotype and induces muscle atrophy. Mechanistically, ZFP36L2-AS interacts with acetyl-CoA carboxylase alpha (ACACA) and pyruvate carboxylase (PC) to induce ACACA dephosphorylation and damaged PC protein stability, thus modulating muscle metabolism. Meanwhile, ZFP36L2-AS can activate ACACA to reduce acetyl-CoA content, which enhances the inhibition of PC activity. Our findings present a novel model about the regulation of IncRNA on muscle metabolism.

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