circIGF1R缺失通过海绵miR-362-5p抑制心肌细胞增殖。

IF 2.6 4区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
Jun-Hui Zeng, Hong-Ji Li, Kun Liu, Chi-Qian Liang, Hai-Yan Wu, Wu-Yun Chen, Ming-Hui Tang, Wan-Ling Zhao, Dong-Qing Cai, Xu-Feng Qi
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引用次数: 0

摘要

环状rna (circRNAs)通常由前体mRNA的反剪接形成。越来越多的证据表明环状rna在心血管疾病中的重要作用。然而,环胰岛素样生长因子1受体(circIGF1R)在心肌细胞(CM)增殖中的作用尚不清楚。在这里,我们研究了circIGF1R在CMs增殖中的潜在作用。我们发现circIGF1R在成年小鼠心脏组织和原代CMs中的表达在出生后1天显著低于新生小鼠(p1)。在切除后0.5天和1天,在受损新生儿心脏中检测到circIGF1R表达增加。circIGF1R敲低显著降低原代CMs的增殖。联合预测软件、荧光素酶报告基因分析和定量实时pcr (qPCR)显示circIGF1R与miR-362-5p相互作用。与新生儿心脏相比,miR-362-5p在成人心脏中的表达显著增加。此外,心脏损伤显著降低了新生小鼠miR-362-5p的表达。miR-362-5p模拟物显著抑制原代CMs的增殖,而miR-362-5p的敲低促进了CMs的增殖。同时,miR-362-5p沉默可以挽救circIGF1R敲低诱导的CMs的增殖抑制。靶标预测和qPCR验证显示,miR-362-5p在原代CMs中显著抑制Phf3的表达。此外,与新生儿心脏相比,成人心脏中Phf3的表达降低。与假心脏相比,损伤新生儿心脏中Phf3的表达增加。敲低Phf3可显著抑制CMs的增殖。综上所述,这些发现提示circIGF1R可能通过海绵化miR-362-5p促进Pfh3的表达,从而促进心肌细胞增殖,为心脏再生调控提供了重要的实验依据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Loss of circIGF1R Suppresses Cardiomyocytes Proliferation by Sponging miR-362-5p.

Circular RNAs (circRNAs) are generally formed by the back-splicing of precursor mRNA. Increasing evidence implicates the important role of circRNAs in cardiovascular diseases. However, the role of circ-insulin-like growth factor 1 receptor (circIGF1R) in cardiomyocyte (CM) proliferation remains unclear. Here, we investigated the potential role of the circIGF1R in the proliferation of CMs. We found that circIGF1R expression in heart tissues and primary CMs from adult mice was significantly lower than that in neonatal mice at postnatal 1 day (p1). Increased circIGF1R expression was detected in the injured neonatal heart at 0.5 and 1 days post-resection. circIGF1R knockdown significantly decreased the proliferation of primary CMs. Combined prediction software, luciferase reporter gene analysis, and quantitative real time-PCR (qPCR) revealed that circIGF1R interacted with miR-362-5p. A significant increase in miR-362-5p expression was detected in the adult heart compared with that in the neonatal heart. Further, heart injury significantly decreased the expression of miR-362-5p in neonatal mice. Treatment with miR-362-5p mimics significantly suppressed the proliferation of primary CMs, whereas knockdown of miR-362-5p promoted the CMs proliferation. Meanwhile, miR-362-5p silencing can rescue the proliferation inhibition of CMs induced by circIGF1R knockdown. Target prediction and qPCR validation revealed that miR-362-5p significantly inhibited the expression of Phf3 in primary CMs. In addition, decreased Phf3 expression was detected in adult hearts compared with neonatal hearts. Consistently, increased Phf3 expression was detected in injured neonatal hearts compared with that in sham hearts. Knockdown of Phf3 markedly repressed CMs proliferation. Taken together, these findings suggest that circIGF1R might contribute to cardiomyocyte proliferation by promoting Pfh3 expression by sponging miR-362-5p and provide an important experimental basis for the regulation of heart regeneration.

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来源期刊
DNA and cell biology
DNA and cell biology 生物-生化与分子生物学
CiteScore
6.60
自引率
0.00%
发文量
93
审稿时长
1.5 months
期刊介绍: DNA and Cell Biology delivers authoritative, peer-reviewed research on all aspects of molecular and cellular biology, with a unique focus on combining mechanistic and clinical studies to drive the field forward. DNA and Cell Biology coverage includes: Gene Structure, Function, and Regulation Gene regulation Molecular mechanisms of cell activation Mechanisms of transcriptional, translational, or epigenetic control of gene expression Molecular Medicine Molecular pathogenesis Genetic approaches to cancer and autoimmune diseases Translational studies in cell and molecular biology Cellular Organelles Autophagy Apoptosis P bodies Peroxisosomes Protein Biosynthesis and Degradation Regulation of protein synthesis Post-translational modifications Control of degradation Cell-Autonomous Inflammation and Host Cell Response to Infection Responses to cytokines and other physiological mediators Evasive pathways of pathogens.
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