Loss of circIGF1R Suppresses Cardiomyocytes Proliferation by Sponging miR-362-5p

作者：Junhui Zeng, Hongji Li, Kun Liu, Chi‐Qian Liang, Haiyan Wu, Wu-Yun Chen, Minghui Tang, Wanling Zhao, Dongqing Cai, Xufeng Qi · 发表于：DNA and Cell Biology · 年份：2023 · DOI：10.1089/dna.2022.0590 · 被引用次数：2 · 研究领域：Circular RNAs in diseases、Cancer-related molecular mechanisms research、MicroRNA in disease regulation

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 C...