Inhibiting microRNA-155 attenuates atrial fibrillation by targeting CACNA1C

Wang, Jiangang; Ye, Qing; Bai, Shuyun; Chen, Pengfei; Zhao, Yichen; Ma, Xiaolong; Bai, Caiquan; Yang, Lei; Meng, Xia; Zeng, Caiwu; Liu, Quan; Zhao, Cheng; Yao, Yan

doi:10.1016/j.yjmcc.2021.02.008

Cited by 21 publications

(14 citation statements)

References 31 publications

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“…Therefore, the results may be unpersuasive to some extent. In future, human-induced pluripotent stem cell-derived atrial cardiomyocytes (hiPSC-aCMs) [26] need to be used to confirm the results in this study. In addition, rat cardiomyocyte cell line H9C2 and neonatal mouse cardiac myocytes need to be used to verify the role of the circ_ 0023461/miR-370-3p/PDE4D axis in other species in vitro, and AMI rat or mouse model in vivo needs to be established by ligating the coronary artery to further confirm the results in this study.…”

Section: Discussionmentioning

confidence: 58%

circ_0023461 Silencing Protects Cardiomyocytes from Hypoxia‐Induced Dysfunction through Targeting miR‐370‐3p/PDE4D Signaling

Ren

Jiang

et al. 2021

Oxidative Medicine and Cellular Longevity

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Background. Acute myocardial infarction (AMI) is a common cardiovascular disease with high disability and mortality. Circular RNAs (circRNAs) are implicated in the pathomechanism of multiple human diseases, including AMI. This study intended to explore the function and working mechanism of a novel circRNA circ_0023461 in hypoxia-induced cardiomyocytes. Methods. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blot assay were implemented to detect RNA and protein expression. Cell counting kit-8 (CCK8) assay and 5-ethynyl-2 ′ -deoxyuridine (Edu) assay were conducted to analyze cell viability and proliferation ability. Cell migration and apoptosis were assessed by Transwell assay and flow cytometry. Cell oxidative stress was analyzed using the commercial kits. Enzyme-linked immunosorbent assay (ELISA) was conducted to analyze cell inflammation. Cell glycolytic metabolism was evaluated using the commercial kits. Dual-luciferase reporter assay and RNA pull-down assay were conducted to verify the intermolecular interactions. Results. circ_0023461 expression was upregulated in AMI patients and hypoxia-induced AC16 cells. Hypoxia restrained the viability, proliferation, migration, and glycolysis and induced the apoptosis, oxidative stress, and inflammation of AC16 cells, and these effects were attenuated by the silence of circ_0023461. MicroRNA-370-3p (miR-370-3p) was verified as a target of circ_0023461, and circ_0023461 silencing-mediated protective effects in hypoxia-induced cardiomyocytes were partly alleviated by the knockdown of miR-370-3p. miR-370-3p interacted with the 3 ′ untranslated region (3 ′ UTR) of phosphodiesterase 4D (PDE4D), and PDE4D overexpression partly reversed miR-370-3p overexpression-induced protective effects in hypoxia-induced cardiomyocytes. circ_0023461 can upregulate PDE4D expression by acting as a molecular sponge for miR-370-3p in AC16 cells. Conclusion. circ_0023461 knockdown attenuated hypoxia-induced dysfunction in AC16 cells partly by targeting the miR-370-3p/PDE4D axis.

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Section: Discussionmentioning

confidence: 58%

circ_0023461 Silencing Protects Cardiomyocytes from Hypoxia‐Induced Dysfunction through Targeting miR‐370‐3p/PDE4D Signaling

Ren

Jiang

et al. 2021

Oxidative Medicine and Cellular Longevity

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“…The characterization of hiPSC‐aCMs was described before. 17 Figure 3A shows the hiPSC‐aCMs‐fibroblast contact co‐culture. The beating of myocytes was crucial when distinguishing the hiPSC‐aCMs from fibroblasts ( Supplementary Video ).…”

Section: Resultsmentioning

confidence: 99%

“…An early conducted research has documented a highly homogenous atrial‐like cardiomyocytes (aCMs) obtained from human pluripotent stem cells. 16 , 17 Details are shown in the Supplemental Materials .…”

Section: Methodsmentioning

confidence: 99%

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MicroRNA‐146b‐5p promotes atrial fibrosis in atrial fibrillation by repressing TIMP4

Liu

et al. 2021

J Cellular Molecular Medi

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“…Recently, a gene therapy trial produced an inspiring result, that gene therapy with KCNH2 could eliminate AF via prolonging atrial action potential duration (71). Numerous studies suggest that SIRT1, VCAM, VEGFA, TGFB1, CAP3, and CACNA1C are involved in the progress of the occurrence, development, and treatment of AF (72)(73)(74)(75)(76).…”

Section: Discussionmentioning

confidence: 99%

Potential Mechanism of Dingji Fumai Decoction Against Atrial Fibrillation Based on Network Pharmacology, Molecular Docking, and Experimental Verification Integration Strategy

Liang

Wen

et al. 2021

Front. Cardiovasc. Med.

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Background: Dingji Fumai Decoction (DFD), a traditional herbal mixture, has been widely used to treat arrhythmia in clinical practice in China. However, the exploration of the active components and underlying mechanism of DFD in treating atrial fibrillation (AF) is still scarce.Methods: Compounds of DFD were collected from TCMSP, ETCM, and literature. The targets of active compounds were explored using SwissTargetPrediction. Meanwhile, targets of AF were collected from DrugBank, TTD, MalaCards, TCMSP, DisGeNET, and OMIM. Then, the H-C-T-D and PPI networks were constructed using STRING and analyzed using CytoNCA. Meanwhile, VarElect was utilized to detect the correlation between targets and diseases. Next, Metascape was employed for systematic analysis of the mechanism of potential targets and protein complexes in treating AF. AutoDock Vina, Pymol, and Discovery Studio were applied for molecular docking. Finally, the main findings were validated through molecular biology experiments.Results: A total of 168 active compounds and 1,093 targets of DFD were collected, and there were 89 shared targets between DFD and AF. H-C-T-D network showed the relationships among DFD, active compounds, targets, and AF. Three functional protein complexes of DFD were extracted from the PPI network. Further systematic analysis revealed that the regulation of cardiac oxidative stress, cardiac inflammation, and cardiac ion channels were the potential mechanism of DFD in treating AF. Addtionally, molecular docking verified the interactions between active compounds and targets. Finally, we found that DFD significantly increased the level of SIRT1 and reduced the levels of ACE, VCAM-1, and IL-6.Conclusions: DFD could be utilized in treating AF through a complicated mechanism, including interactions between related active compounds and targets, promoting the explanation and understanding of the molecular biological mechanism of DFD in the treatment of AF.

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Inhibiting microRNA-155 attenuates atrial fibrillation by targeting CACNA1C

Cited by 21 publications

References 31 publications

circ_0023461 Silencing Protects Cardiomyocytes from Hypoxia‐Induced Dysfunction through Targeting miR‐370‐3p/PDE4D Signaling

circ_0023461 Silencing Protects Cardiomyocytes from Hypoxia‐Induced Dysfunction through Targeting miR‐370‐3p/PDE4D Signaling

MicroRNA‐146b‐5p promotes atrial fibrosis in atrial fibrillation by repressing TIMP4

Potential Mechanism of Dingji Fumai Decoction Against Atrial Fibrillation Based on Network Pharmacology, Molecular Docking, and Experimental Verification Integration Strategy

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