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miR-7 通过 基因调控鸡原代成肌细胞的凋亡。

miR-7 regulates the apoptosis of chicken primary myoblasts through the gene.

机构信息

College of Animal Science and Technology, Yangzhou University, Yangzhou, China.

Institute of Animal Science, Chinese Academy of Agricultral Sciences, Beijing, China.

出版信息

Br Poult Sci. 2022 Feb;63(1):39-45. doi: 10.1080/00071668.2021.1958299. Epub 2021 Aug 13.

Abstract
  1. MicroRNAs (miRNAs) play a vital role in the proliferation, differentiation, and apoptosis of myoblasts. However, the effect of miR-7 on the apoptosis of chicken primary myoblasts (CPMs) and its mechanism is still unclear.2. In this study, the expression of apoptosis marker genes () in CPMs was significantly increased after transfection of miR-7 mimic. The expression of the apoptosis marker genes in CPMs was significantly reduced after transfection with miR-7 inhibitor. Flow cytometry showed that the late apoptosis rate of the mimic group was significantly higher than the negative control (NC). The viable cells of the mimic group were significantly lower than the NC. In contrast, inhibition of miR-7 had the opposite effect.3. The dual-luciferase assay showed that the was a target gene of miR-7. The rescue experiment showed that the gene could attenuate the effect of miR-7 on the expression of apoptosis marker genes in CPMs.4. Determination of the function the gene showed that the expression of the apoptosis marker genes in CPMs decreased significantly compared with the NC after its overexpression. Inhibition of gene had the opposite effect. Flow cytometry showed that overexpression of the gene inhibited early apoptosis of myoblasts (P ≤ 0.01), while interference with the gene could promote early apoptosis of myoblasts (P ≤ 0.001).5. The results demonstrated, for the first time, that miR-7 promotes apoptosis in chicken primary myoblasts by regulating the expression of the gene.
摘要
  1. 微小 RNA(miRNAs)在成肌细胞的增殖、分化和凋亡中发挥着重要作用。然而,miR-7 对鸡原代成肌细胞(CPM)凋亡的影响及其机制尚不清楚。

  2. 在本研究中,转染 miR-7 模拟物后,CPM 中转录的凋亡标记基因的表达显著增加。转染 miR-7 抑制剂后,凋亡标记基因在 CPMs 中的表达显著降低。流式细胞术显示,模拟组的晚期凋亡率明显高于阴性对照组(NC)。模拟组的活细胞数明显低于 NC。相反,抑制 miR-7 则产生相反的效果。

  3. 双荧光素酶报告基因实验表明,是 miR-7 的靶基因。挽救实验表明,抑制 miR-7 可以减弱其对 CPMs 中凋亡标记基因表达的影响。

  4. 目的基因功能的确定表明,过表达后 CPMs 中转录的凋亡标记基因的表达明显低于 NC。抑制目的基因则产生相反的效果。流式细胞术显示,过表达目的基因可显著抑制成肌细胞的早期凋亡(P ≤ 0.01),而抑制目的基因则可促进成肌细胞的早期凋亡(P ≤ 0.001)。

  5. 这些结果首次表明,miR-7 通过调节 基因的表达促进鸡原代成肌细胞的凋亡。

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