The deficiency of miR-214-3p exacerbates cardiac fibrosis via miR-214-3p/NLRC5 axis

Yang, Kun; Shi, Jiaran; Hu, Zhujun; Hu, Xinyang

doi:10.1042/cs20190203

Cited by 35 publications

(19 citation statements)

References 31 publications

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“…For example, miR-214-3p regulated the tumorigenesis of ovarian cancer, endometrial cancer, and papillary thyroid carcinoma ( Fang et al, 2019 ; Yang C. et al, 2019 ; Sui et al, 2020 ). MiR-214-3p was identified to repress cardiac fibrosis through the inhibition of the NOD-like receptor family CARD domain containing 5 ( Yang K. et al, 2019 ). In addition, miR-214-3p expression was downregulated in the rat model of spinal nerve ligation, and the elevated miR-214-3p expression mitigated neuroinflammation and neuropathic pain by targeting colony-stimulating factor-1 ( Yang K. et al, 2019 ).…”

Section: Discussionmentioning

confidence: 99%

“…MiR-214-3p was identified to repress cardiac fibrosis through the inhibition of the NOD-like receptor family CARD domain containing 5 ( Yang K. et al, 2019 ). In addition, miR-214-3p expression was downregulated in the rat model of spinal nerve ligation, and the elevated miR-214-3p expression mitigated neuroinflammation and neuropathic pain by targeting colony-stimulating factor-1 ( Yang K. et al, 2019 ). MiR-214-3p also associated with the neuroprotection of Sigma 1 receptor in retinitis pigmentosa ( Wang and Smith, 2019 ).…”

Section: Discussionmentioning

confidence: 99%

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Knockdown of SNHG14 Alleviates MPP+-Induced Injury in the Cell Model of Parkinson’s Disease by Targeting the miR-214-3p/KLF4 Axis

et al. 2020

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Background: Parkinson's disease (PD) is the second most common neurodegenerative disease. Long non-coding RNA (lncRNA) small nucleolar RNA host gene 14 (SNHG14) has been demonstrated as an important regulator in PD pathology. However, the functional mechanisms played by SNHG14 in PD remain largely unclear. Methods: We used 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 1methyl-4-phenylpyridinium (MPP +) to establish PD mouse and cell models. The levels of SNHG14, miR-214-3p, and Krüppel-like factor 4 (KLF4) were gauged by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot analysis. Cell viability and apoptosis were determined using the Cell Counting-8 Kit (CCK-8) assay and flow cytometry, respectively. The levels of inflammatory cytokines were evaluated by ELISA. The relationships among SNHG14, miR-214-3p, and KLF4 were confirmed by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Results: Our data indicated that SNHG14 was upregulated and miR-214-3p was downregulated in PD models. SNHG14 knockdown ameliorated MPP +-stimulated damage in SK-N-SH cells, as evidenced by the enhancement in cell viability and the suppression in cell apoptosis and pro-inflammatory cytokine production. Mechanistically, SNHG14 directly targeted miR-214-3p via binding to miR-214-3p, and SNHG14 knockdown protected SK-N-SH cell from MPP +-stimulated cytotoxicity by upregulating miR-214-3p. KLF4 was a direct target of miR-214-3p, and SNHG14 regulated KLF4 expression by acting as a miR-214-3p sponge. Furthermore, miR-214-3p overexpression alleviated MPP +-stimulated damage in SK-N-SH cells by downregulating KLF4. Conclusion: Our current study first demonstrated the protective effect of SNHG14 knockdown on MPP +-stimulated cytotoxicity in SK-N-SH cells at least partially by targeting the miR-214-3p/KLF4 axis, illuminating a promising target for PD intervention and treatment.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Knockdown of SNHG14 Alleviates MPP+-Induced Injury in the Cell Model of Parkinson’s Disease by Targeting the miR-214-3p/KLF4 Axis

et al. 2020

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“…S100 calcium binding protein A4 ( S100a4 ), also known as fibroblast-specific protein-1 (FSP1), is expressed exclusively in fibroblast cells. The S100a4-Cre mouse line expresses Cre recombinase driven by the mouse S100a4 promoter, and it has been previously used for the generation of cardiac fibroblast-specific gene knockout mice 28 , 29 . We crossbred Fcer1a flox/flox mice (C57BL/6, N9) with S100a4-Cre mice to generate Fcer1a flox/- Cre +/- mice.…”

Section: Methodsmentioning

confidence: 99%

Elevated IgE promotes cardiac fibrosis by suppressing miR-486a-5p

Zhao¹,

Yang²,

Geng³

et al. 2021

Theranostics

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Rationale: Cardiac fibrosis is an important feature of cardiac remodeling and is a hallmark of heart failure. Recent studies indicate that elevated IgE plays a causal role in pathological cardiac remodeling. However, the underlying mechanism of how IgE promotes cardiac fibrosis has not been fully elucidated. Methods and Results: To explore the function of IgE in cardiac fibrosis, we stimulated mouse primary cardiac fibroblasts (CFs) with IgE and found that both IgE receptor (FcεR1) and fibrosis related proteins were increased after IgE stimulation. Specific deletion of FcεR1 in CFs alleviated angiotensin II (Ang II)-induced cardiac fibrosis in mice. To investigate the mechanisms underlying the IgE-mediated cardiac fibrosis, deep miRNA-seq was performed. Bioinformatics and signaling pathway analysis revealed that IgE upregulated Col1a1 and Col3a1 expression in CFs by repressing miR-486a-5p, with Smad1 participating downstream of miR-486a-5p in this process. Lentivirus-mediated overexpression of miR-486a-5p was found to alleviate Ang II-induced myocardial interstitial fibrosis in mice. Moreover, miR-486-5p serum levels were lower in patients with heart failure than in healthy controls, and were negatively correlated with NT-proBNP levels. Conclusions: Our study demonstrates that elevated IgE promotes pathological cardiac fibrosis by modulating miR-486a-5p and downstream factors, such as Smad1 . These findings suggest new targets for pathological cardiac fibrosis intervention.

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“…[ 43 ] Yang et al showed that has-miR-214-3p deficiency exacerbated cardiac fibrosis. [ 44 ] The downregulation of miR-214-3p expression inhibited the proliferation and invasion of HCC cells [ 45 ] and inhibited the progression of HCC by directly downregulating MELK expression. [ 46 ] Consistent with previous studies, our study indicated that miR-214-3p is downregulated by 2-fold in HCC and may affect HCC prognosis by directly regulating downstream target genes.…”

Section: Discussionmentioning

confidence: 99%

Integrated analysis of ceRNA network in hepatocellular carcinoma using bioinformatics analysis

Luo¹,

Li²,

Huang³

et al. 2021

Medicine

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Background: Long noncoding RNAs (lncRNAs) can work as microRNA (miRNA) sponges through a competitive endogenous RNA (ceRNA) mechanism. LncRNAs and miRNAs are important components of competitive endogenous binding, and their expression imbalance in hepatocellular carcinoma (HCC) is closely related to tumor development, diagnosis, and prognosis. This study explored the potential impact of the ceRNA regulatory network in HCC on the prognosis of HCC patients. Methods: We thoroughly researched the differential expression profiles of lncRNAs, miRNAs, and mRNAs from 2 HCC Gene Expression Omnibus datasets ( GSE98269 and GSE60502 ). Then, a dysregulated ceRNA network was constructed by bioinformatics. In addition, hub genes in the ceRNA network were screened by Cytoscape, these hub genes functional analysis was performed by gene set enrichment analysis, and the expression of these hub genes in tumors and their correlation with patient prognosis were verified with Gene Expression Profiling Interactive Analysis. Results: A ceRNA network was successfully constructed in this study including 4 differentially expressed (DE) lncRNAs, 7 DEmiRNAs, and 166 DEmRNAs. Importantly, 4 core genes ( CCNA2 , CHEK1 , FOXM1 , and MCM2 ) that were significantly associated with HCC prognosis were identified. Conclusions: Our study provides comprehensive and meaningful insights into HCC tumorigenesis and the underlying molecular mechanisms of ceRNA. Furthermore, the specific ceRNAs can be further used as potential therapeutic targets and prognostic biomarkers for HCC.

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The deficiency of miR-214-3p exacerbates cardiac fibrosis via miR-214-3p/NLRC5 axis

Cited by 35 publications

References 31 publications

Knockdown of SNHG14 Alleviates MPP+-Induced Injury in the Cell Model of Parkinson’s Disease by Targeting the miR-214-3p/KLF4 Axis

Knockdown of SNHG14 Alleviates MPP+-Induced Injury in the Cell Model of Parkinson’s Disease by Targeting the miR-214-3p/KLF4 Axis

Elevated IgE promotes cardiac fibrosis by suppressing miR-486a-5p

Integrated analysis of ceRNA network in hepatocellular carcinoma using bioinformatics analysis

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