LincRNA-Cox2 promotes pulmonary arterial hypertension by regulating the let-7a-mediated STAT3 signaling pathway

Cheng, Gesheng; He, Lu; Zhang, Yushun

doi:10.1007/s11010-020-03877-6

Cited by 24 publications

(19 citation statements)

References 38 publications

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“…For example, lincRNA-Cox2 promotes PAH development by regulating the let-7a/STAT3 pathway. 36 MiR-125-5p ameliorates monocrotaline-induced PAH by targeting the transforming growth factor (TGF)-beta1 and interleukin-6/STAT3 signaling pathways. 37 Moreover, our rescue assays proved that miR-328-3p/STAT3 axis was responsible for regulating circHIPK3 in PAH pathogenesis.…”

Section: Discussionmentioning

confidence: 99%

Circular RNA‐HIPK3 regulates human pulmonary artery endothelial cells function and vessel growth by regulating microRNA‐328‐3p/STAT3 axis

Hong¹,

Ma²,

Liu³

et al. 2021

Pulm. circ.

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The proliferation and migration of pulmonary artery endothelial cells are the pathological basis of pulmonary vascular remodeling with pulmonary hypertension. Recent studies have shown that circular RNA (circRNA) regulates biological processes in various vascular diseases, including pulmonary arterial hypertension (PAH). It has been reported that CircRNA regulates the vascular endothelial cellsâ function. Therefore, circRNA may have crucial roles in pulmonary artery endothelial cells (hPAECs) proliferation, migration, and tube formation in PAH. In this study, we aimed to discover the role and mechanism of circHIPK3 in the proliferation and migration of pulmonary hypertension hPAECs. First, we used platelet-derived growth factor (PDGF) âstimulated hPAECs as a cellular model of PAH. The results showed that PDGF promoted hPAECs proliferation, migration, and tube formation. Notably, PDGF upregulated the expression of circHIPK3 in hPAECs and regulated their proliferation, migration, and angiogenesis. Mechanistically, we confirmed miR-328-3p was copiously pulled down by circHIPK3 in hPAECs. Luciferase reporter and RNA immunoprecipitation assays further indicated the cytoplasmic interactions between circHIPK3 and miR-328-3p. Subsequently, we found that circHIPK3 might increase the expression of STAT3 by sponging miR-328-3p. Collectively, our results demonstrated that the circHIPK3-miR-328-3p-STAT3 axis contributed to the pathogenesis of PAH by stimulating hPAECs proliferation, migration, and angiogenesis. The circHIPK3 has an accelerated role in PAH development, implicating the potential values of circHIPK3 in PAH therapy.

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Section: Discussionmentioning

confidence: 99%

Circular RNA‐HIPK3 regulates human pulmonary artery endothelial cells function and vessel growth by regulating microRNA‐328‐3p/STAT3 axis

Hong¹,

Ma²,

Liu³

et al. 2021

Pulm. circ.

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“…Another lncRNA, lincRNA-Cox2, has been described as a regulator of inflammation, involved in atherosclerosis, and also found to be involved in PASCM migration and proliferation. LincRNA-Cox2 sponges miR-let-7a and leads to an increase in STAT3 [195]. In patient peripheral blood samples, lincRNA-Cox2 is upregulated, which is also observed in vitro in hypoxic PASMCs, and its silencing leads to decreased cell proliferation and migration.…”

Section: Non-coding Rnas Involved In Pahmentioning

confidence: 95%

Epigenetic Regulation of Pulmonary Arterial Hypertension-Induced Vascular and Right Ventricular Remodeling: New Opportunities?

Kocken

Martins

2020

IJMS

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Pulmonary artery hypertension (PAH) is a rare chronic disease with high impact on patients’ quality of life and currently no available cure. PAH is characterized by constant remodeling of the pulmonary artery by increased proliferation and migration of pulmonary arterial smooth muscle cells (PASMCs), fibroblasts (FBs) and endothelial cells (ECs). This remodeling eventually leads to increased pressure in the right ventricle (RV) and subsequent right ventricle hypertrophy (RVH) which, when left untreated, progresses into right ventricle failure (RVF). PAH can not only originate from heritable mutations, but also develop as a consequence of congenital heart disease, exposure to drugs or toxins, HIV, connective tissue disease or be idiopathic. While much attention was drawn into investigating and developing therapies related to the most well understood signaling pathways in PAH, in the last decade, a shift towards understanding the epigenetic mechanisms driving the disease occurred. In this review, we reflect on the different epigenetic regulatory factors that are associated with the pathology of RV remodeling, and on their relevance towards a better understanding of the disease and subsequently, the development of new and more efficient therapeutic strategies.

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“…Wang et al [334] found that the altered expression of hsa-mir-657 in GDM. Improta Caria et al [335], Li et al [336], Park et al [337], Cheng et al [338] and Davis, [339] demonstrated that hsa-mir-657, BMI1, GATA4, STAT3 and ATF3 played a pivotal role in the hypertension, but these miRNAs might be novel targets for GDM. Improta Caria et al [335], Patankar et al [340], Bochkis et al [341], Nishimura et al [342], Su et al [343] and Kim et al [344] suggested that hsa-mir-657, GATA4, FOXA2, EP300, STAT3 and ATF3 could induce obesity, but these genes might be novel targets for GDM.…”

Section: Discussionmentioning

confidence: 99%

Identification of differentially expressed genes and signaling pathways in gestational diabetes mellitus by integrated bioinformatics analysis

Vastrad¹,

Vastrad²

2021

Preprint

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Gestational diabetes mellitus (GDM) is a metabolic disorder during pregnancy. Numerous biomarkers have been identified that are linked with the occurrence and development of GDM. The aim of this investigation was to identify differentially expressed genes (DEGs) in GDM using a bioinformatics approach to elucidate their molecular pathogenesis. GDM associated expression profiling by high throughput sequencing dataset (GSE154377) was obtained from Gene Expression Omnibus (GEO) database including 28 normal pregnancy samples and 33 GDM samples. DEGs were identified using DESeq2. The gene ontology (GO) and REACTOME pathway enrichments of DEGs were performed by g:Profiler. Protein-protein interaction (PPI) networks were assembled with Cytoscape software and separated into modules using the PEWCC1 algorithm. MiRNA-hub gene regulatory network and TF-hub gene regulatory network were performed with the miRNet database and NetworkAnalyst database. Receiver Operating Characteristic (ROC) analyses was conducted to validate the hub genes. A total of 953 DEGs were identified, of which 478 DEGs were up regulated and 475 DEGs were down regulated. Furthermore, GO and REACTOME pathway enrichment analysis demonstrated that these DEGs were mainly enriched in multicellular organismal process, cell activation, formation of the cornified envelope and hemostasis. TRIM54, ELAVL2, PTN, KIT, BMPR1B, APP, SRC, ITGA4, RPA1 and ACTB were identified as key genes in the PPI network, miRNA-hub gene regulatory network and TF-hub gene regulatory network. TRIM54, ELAVL2, PTN, KIT, BMPR1B, APP, SRC, ITGA4, RPA1 and ACTB in GDM were validated using ROC analysis. This investigation provides further insights into the molecular pathogenesis of GDM, which might facilitate the diagnosis and treatment of GDM.

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LincRNA-Cox2 promotes pulmonary arterial hypertension by regulating the let-7a-mediated STAT3 signaling pathway

Cited by 24 publications

References 38 publications

Circular RNA‐HIPK3 regulates human pulmonary artery endothelial cells function and vessel growth by regulating microRNA‐328‐3p/STAT3 axis

Circular RNA‐HIPK3 regulates human pulmonary artery endothelial cells function and vessel growth by regulating microRNA‐328‐3p/STAT3 axis

Epigenetic Regulation of Pulmonary Arterial Hypertension-Induced Vascular and Right Ventricular Remodeling: New Opportunities?

Identification of differentially expressed genes and signaling pathways in gestational diabetes mellitus by integrated bioinformatics analysis

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