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Sci Rep:研究确定lincRNA Paral1为脂肪细胞分化机功能的敏感调节因子

2017-11-02 MedSci MedSci原创

脂肪细胞分化和功能依赖于转录因子网络,而在肥胖相关的低级别慢性炎症中被破坏,导致脂肪组织功能障碍。在这种情况下,需要彻底了解脂肪组织病理生理学中涉及的转录调控网络。基因组功能注释的最新进展突出了非编码RNAs在细胞分化过程中与转录因子协调的作用。使用无偏差的全基因组方法,研究人员确定并表征了脂肪细胞分化期间明显诱导的新型长链非编码RNA(lincRNA)。这种lincRNA有利于脂肪细胞的分化,并

脂肪细胞分化和功能依赖于转录因子网络,而在肥胖相关的低级别慢性炎症中被破坏,导致脂肪组织功能障碍。在这种情况下,需要彻底了解脂肪组织病理生理学中涉及的转录调控网络。基因组功能注释的最新进展突出了非编码RNAs在细胞分化过程中与转录因子协调的作用。

使用无偏差的全基因组方法,研究人员确定并表征了脂肪细胞分化期间明显诱导的新型长链非编码RNA(lincRNA)。这种lincRNA有利于脂肪细胞的分化,并通过与paraspeckle组分和hnRNP样RNA结合蛋白14(RBM14/NCoAA)相互作用共同激活成脂调节过氧化物酶体增殖物激活受体γ(PPARγ),因此被称为PPARγ-激活剂RBM14相关lncRNA(Paral1)。Paral1表达仅限于脂肪细胞,随着体重指数的增加而下降。在饮食诱导或遗传小鼠肥胖模型中也观察到Paral1的表达降低,且体外TNF处理模拟了此下调。

总之,该研究结果确定了脂肪转录调控网络的一个新的组成部分,将lincRNA Paral1定义为脂肪细胞分化和功能的肥胖敏感调节因子。

原始出处:

François F. Firmin, Frederik Oger, et al., The RBM14/CoAA-interacting, long intergenic non-coding RNA Paral1 regulates adipogenesis and coactivates the nuclear receptor PPARγ. Sci Rep. 2017; 7: 14087. Published online 2017 Oct 26. doi: 10.1038/s41598-017-14570-y

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    2018-08-21 zutt
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