Key result
AF is linked to increased miR-24 expression, reduced LINC00472 expression, and increased LINC00472 DNA methylation.
Why the study?
Deregulation of RyR2 may contribute to atrial fibrillation pathogenesis, and the authors aimed to investigate the role of lncRNA LINC00472 in AF pathogenesis.
Case-Control (n=293)
LINC00472 appears to play a role in the pathogenesis of atrial fibrillation by modulating the miR-24/JP2/RyR2 signaling pathway.
Supports further exploration of LINC00472-miR-24 in AF pathogenesis; leaves open any clinical implications without prospective validation.
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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Wang et al. (2019) conducted a case-control in Atrial fibrillation (n=293). Atrial fibrillation vs. Healthy controls was evaluated on Expression levels of miR-24, LINC00472, JP2 and RyR2. Atrial fibrillation patients had increased miR-24 expression, reduced LINC00472 expression, and increased LINC00472 DNA methylation compared to healthy controls.
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