例如:"lncRNA", "apoptosis", "WRKY"

A new miRNA regulator, miR-672, reduces cardiac hypertrophy by inhibiting JUN expression.

Gene. 2018 Mar 30;648:21-30. Epub 2018 Jan 12
Yili Lu 1 , Fangli Wu 2
Yili Lu 1 , Fangli Wu 2

[No authors listed]

Author information
  • 1 Department of Pediatrics, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325027, China.
  • 2 Key Laboratory of Plant Secondary Metabolism and Regulation of Zhejiang Province, College of Life Sciences, Zhejiang Sci-Tech University, Hangzhou 310018, China. Electronic address: wfl@zstu.edu.cn.

摘要


Cardiac hypertrophy is one of the initial symptoms of many heart diseases. We found that miR-672-5p may participate in the regulation of heart disease development in mouse, but the association between miR-672-5p and cardiac hypertrophy remains unclear. In the present study, we found that the abundance of miR-672-5p decreased in hypertrophic cardiomyocytes induced by phenylephrine, angiotensin II (Ang II) and insulin-like growth factor 1. Putative target genes of miR-672-5p were identified using four pipelines, miRWalk, miRanda, RNA22 and Targetscan, and a total of 834 genes were predicted by all four pipelines. Among these target genes, 98 were associated with the development of heart disease. PPI networks showed that the Jun proto-oncogene product (JUN), a subunit of the AP-1 transcription factor, had the highest node degree, and it was defined as the hub gene of the PPI networks. Luciferase assays showed that miR-672-5p bound to the of the JUN gene and decreased luciferase activity, indicating that JUN is a target of miR-672-5p. Finally, we found that increasing the abundance of miR-672-5p in cardiomyocytes controlled the relative cell area in Ang II-stimulated hypertrophic cardiomyocytes. Correspondingly, the abundance of JUN, a target of miR-672-5p, was decreased in hypertrophic cardiomyocytes on both mRNA and protein levels, implying that miR-672-5p had suppressive effects on cardiac hypertrophy through regulating the expression of Jun in cardiomyocytes.

KEYWORDS: Cardiac hypertrophy, Differential expression, Mouse, Target genes, miR-672-5p