Chloride Channels are Involved in the Development of Atrial Fibrillation – A Transcriptomic and proteomic Study

Jiang, Yiyao; Hou, Hongying; Yang, Qin; Liu, Xiaocheng; He, Guo‐Wei

doi:10.1038/s41598-017-10590-w

Cited by 22 publications

(25 citation statements)

References 48 publications

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“…MiR-130b-3p was upregulated in RA samples in line with a previous study [31]. MiR-130b-3p is predicted to bind 15 of our down-regulated genes, amongst those there are CACNA2D2 and SLC7A11 which have been reported as down-regulated in AF transcriptomics studies [36,38,67]. CACNA2D2 is a subunit of the voltage-gated calcium channel that modulates the calcium signalling response in cardiomyocytes and induces arrhythmia when down-regulated [68].…”

Section: Plos Onesupporting

confidence: 82%

“…These inconsistencies might reflect 1) heterogeneity between tissue samples (location and collection method), 2) AF type and duration, 3) variation in patient cohorts (comorbidities, life-style, age, medication), and 4) the experimental technique selected to study transcript changes. In fact, our RNA-seq results overlap best with gene expression profiling studies from Jiang et al using similar tissue samples and experiments [38]. A continuous effort from experts to study larger cohorts and collect similar datasets will allow a combined analysis of multiple samples from AF patients and help on accurate selection of target genes and regulatory networks involving miRNAs.…”

Section: Plos Onesupporting

confidence: 52%

“…MiR-338-5p targeted 14 of our DEGs, including IGFBP2, LBH and NPPA. IGFBP2 and LBH have both been reported as up-regulated in three different AF studies and they are increased by 8 and 3 FC in our RA samples, respectively [36][37][38]40]. Mutations in NPPA have been associated with familial AF [61].…”

Section: Plos Onementioning

confidence: 48%

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Investigating gene-microRNA networks in atrial fibrillation patients with mitral valve regurgitation

et al. 2020

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Background Atrial fibrillation (AF) is predicted to affect around 17.9 million individuals in Europe by 2060. The disease is associated with severe electrical and structural remodelling of the heart, and increased the risk of stroke and heart failure. In order to improve treatment and find new drug targets, the field needs to better comprehend the exact molecular mechanisms in these remodelling processes. Objectives This study aims to identify gene and miRNA networks involved in the remodelling of AF hearts in AF patients with mitral valve regurgitation (MVR). Methods Total RNA was extracted from right atrial biopsies from patients undergoing surgery for mitral valve replacement or repair with AF and without history of AF to test for differentially expressed genes and miRNAs using RNA-sequencing and miRNA microarray. In silico predictions were used to construct a mRNA-miRNA network including differentially expressed mRNAs and miRNAs. Gene and chromosome enrichment analysis were used to identify molecular pathways and high-density AF loci. Results We found 644 genes and 43 miRNAs differentially expressed in AF patients compared to controls. From these lists, we identified 905 pairs of putative miRNA-mRNA interactions, including 37 miRNAs and 295 genes. Of particular note, AF-associated miR-130b-3p, miR-338-5p and miR-208a-3p were differentially expressed in our AF tissue samples. These miRNAs are predicted regulators of several differentially expressed genes associated with

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Section: Plos Onesupporting

confidence: 82%

Section: Plos Onesupporting

confidence: 52%

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Investigating gene-microRNA networks in atrial fibrillation patients with mitral valve regurgitation

et al. 2020

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“…Downregulation of CLIC4 also reduced TGF-β1-induced expression of ECM components in primary fibroblasts [25]. In the development of atrial fibrillation, CLIC 1, 4, and 5 played an important role by interacting with collagen IV [26,27].…”

Section: Discussionmentioning

confidence: 96%

“…ClC-2 gene knockout inhibited TGF-β1-induced HConF collagen synthesis and collagen gel contraction. Multiple studies have shown that chloride channels are involved in collagen synthesis [24][25][26]. Qi et al [24] showed that the chloride channel blocker DIDS inhibited the collagen release of HFL1 fibroblasts.…”

Section: Discussionmentioning

confidence: 99%

Role of the ClC-2 Chloride Channel in TGF-β1-induced Proliferation, Collagen Synthesis, and Collagen Gel Contraction Mediated by Human Conjunctival Fibroblasts

Sun¹,

Chui²,

Meng³

et al. 2020

Preprint

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Background: Excessive scar tissue can reduce postoperative survival of filtering blebs in patients with glaucoma. Previous studies have highlighted the role of chloride channels in wound healing. whereas The role of chloride channels in the formation of follicular scar has not been studied. Objectives: To investigate the effects of the ClC-2 chloride channel on scar formation of filtering blebs after glaucoma filtering surgery. Methods: We Inhibited ClC-2 chloride channels of Human Conjunctival Fibroblasts (HConFs) by transfecting HConFs with ClC-2 siRNA, Then cell proliferation, cycle and collagen synthesis of HConFs were measured. ClC-2 siRNA-transfected HConFs were cultured in type I collagen gels in the presence of transforming growth factor (TGF)-β1. Collagen gel contraction was evaluated based on the gel area. The expression levels of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) in HConFs were assessed by western blotting and q-PCR. Results: TGF-β1induced cell proliferation, cell cycle progression, collagen synthesis, and collagen gel contraction in HConFs. TGF-β1 increased MMP-2 and MMP-9 levels but inhibited the expression of TIMPs. ClC-2 siRNA transfection inhibited TGF-β1-induced cell proliferation, cell cycle progression, collagen synthesis, and collagen gel contraction, mediated by HConFs. TGF-β1-induced increases in MMP-2 and MMP-9 were also inhibited by NPPB and ClC-2 siRNA transfection, but TIMP expression was increased by ClC-2 siRNA transfection. Conclusions: These findings demonstrate that ClC-2 gene knockout inhibited TGF-β1-induced cell proliferation, collagen synthesis, and collagen gel contraction of HConFs by attenuating MMP-2 and MMP-9 production and by stimulating TIMP-1 production. Keywords: ClC-2 chloride channel; conjunctival fibroblasts; TGF-β1; wound heal

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MicroRNA‐144‐3p controls the apoptosis of pulmonary artery endothelial cells in pulmonary arterial hypertension via the BMPR2/Smad4 signaling pathway

Shi

Rahman

Liu

et al. 2022

Clinical and Translational Dis

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Chloride Channels are Involved in the Development of Atrial Fibrillation – A Transcriptomic and proteomic Study

Cited by 22 publications

References 48 publications

Investigating gene-microRNA networks in atrial fibrillation patients with mitral valve regurgitation

Investigating gene-microRNA networks in atrial fibrillation patients with mitral valve regurgitation

Role of the ClC-2 Chloride Channel in TGF-β1-induced Proliferation, Collagen Synthesis, and Collagen Gel Contraction Mediated by Human Conjunctival Fibroblasts

MicroRNA‐144‐3p controls the apoptosis of pulmonary artery endothelial cells in pulmonary arterial hypertension via the BMPR2/Smad4 signaling pathway

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