AI Article Synopsis
- Dysregulated methylation of the LINC00472 promoter leads to decreased LINC00472 expression and increased miR-24, which may play a role in atrial fibrillation (AF).
- A study involving 125 AF patients and 168 healthy controls examined the expression levels of miR-24, LINC00472, JP2, and RyR2, and used various laboratory assays to understand their interactions.
- Results indicated that AF patients had higher miR-24 and lower LINC00472 expression, and LINC00472 can influence AF progression through the signaling pathway involving miR-24, JP2, and RyR2.
Article Abstract
Background: Dysregulated methylation of the promoter of lncRNA LINC00472 reduces the expression of LINC00472 and subsequently up-regulates the expression of its competing endogenous RNA miR-24. In addition, JP2 can stabilize the expression of RyR2, whereas the deregulation of RyR2 expression may contribute to the pathogenesis of atrial fibrillation (AF). In this study, we aimed to study the role of LINC00472 in the pathogenesis of AF.
Methods: 125 AF patients and 168 healthy controls were enrolled to compare their expression of miR-24, LINC00472, JP2 and RyR2. A dual-luciferase reporter gene assay accompanied by real-time PCR, Western blot and IHC assay was subsequently conducted to evaluate the regulatory relationship among miR-24, LINC00472, JP2 and RyR2 in HCM and H9C2 cells.
Results: AF patients were associated with an increased level of miR-24 expression and reduced level of LINC00472 expression. Also, the level of DNA methylation in LINC00472 was increased in AF patients. MiR-24 could negatively regulate the expression of LINC00472 and JP2 by directly binding to them.
Conclusions: LINC00472 could regulate the progression of AF via modulating the LINC00472/miR-24/JP2/RyR2 signaling pathway.
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| http://dx.doi.org/10.1016/j.biopha.2019.109364 | DOI Listing |
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