PTEN公司
下调和上调
心肌纤维化
间充质干细胞
癌症研究
心脏纤维化
PI3K/AKT/mTOR通路
纤维化
上皮-间质转换
蛋白激酶B
生物
医学
信号转导
病理
细胞生物学
生物化学
基因
作者
Xianggui Huang,Danling Zheng,Chong Liu,Jianxiang Huang,Xiaoshan Chen,Jialin Zhong,Jing Wang,Xu Lin,Chengkuan Zhao,Meini Chen,Songkun Su,Yun Chen,Chengcheng Xu,Chaoxian Lin,Yihui Huang,Shuyao Zhang
标识
DOI:10.1016/j.intimp.2023.110765
摘要
This study aimed to investigate the role of miR-214 in the bidirectional regulation of p53 and PTEN and its influence on myocardial fibrosis and cardiac mesenchymal transformation in mice with viral myocarditis (VMC). The study established a VMC model in BALB/c mice by injecting them with the CVB3 virus intraperitoneally. Techniques such as ELISA, H&E staining, Masson staining, immunohistochemical staining, RT-qPCR, western blot, and dual-luciferase reporter gene assay were used to detect the expression levels of relevant factors in tissues and cells. Isolation and culture of cardiac fibroblasts (CFs) were also conducted. The study found that miR-214 bidirectional regulation of p53 and PTEN promotes myocardial fibrosis and cardiac mesenchymal transformation in mice with VMC. The expression levels of collagen-related peptides, inflammatory-related factors, miR-214, mesenchymal transformation-related factors, and fibrosis-related factors were significantly increased, while the expression levels of p53, PTEN, and epithelial/endothelial cell phenotype marker factors were significantly decreased. Downregulation of miR-214 or upregulation of p53 and PTEN expression inhibited inflammatory cell and fibroblast infiltration in VMC mouse myocardial tissue. It reduced the proliferation ability while increasing the apoptosis of cardiac fibroblasts. miR-214 plays a significant role in the bidirectional inhibition of p53 and PTEN, which leads to myocardial fibrosis and cardiac mesenchymal transformation in mice with VMC. Downregulation of miR-214 or upregulation of p53 and PTEN expression may provide potential therapeutic targets for treating VMC-induced cardiac fibrosis and mesenchymal transformation.
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