Analysis of miRNA expression profiling in human umbilical vein endothelial cells affected by heat stress

Liu, Jie; Zhu, Guoguo; Xu, Siya; Liu, Shixin; Lu, Qiping; Tang, Zhongzhi

doi:10.3892/ijmm.2017.3174

Cited by 9 publications

(16 citation statements)

References 82 publications

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“…Based on previous miRNA microarray analysis, miR-3613-3p expression levels were decreased in HUVECs under heat stress (19). To confirm the downregulation of miR-3613-3p in heat-treated cells, miR-3613-3p expression was analyzed by RT-qPCR, and the results verified that miR-3613-3p expression was reduced in HS-treated HUVECs compared with control cells (P<0.05; Fig.…”

Section: Resultsmentioning

confidence: 99%

“…For example, miRNA (miR)-155, miR-320, miR-222, miR-125b, miR-410 and miR-218 have been reported to regulate adherens junction disassembly responses, cell migration and cell morphology, contributing to changes in the permeability and integrity of the vasculature (16–18). As underlying regulatory mechanisms such as miRNA expression in response to HS were unknown, miRNA expression was analyzed in our previous study via miRNA microarrays; it was demonstrated that heat stress altered miRNA expression in HUVECs, with 31 miRNAs differing significantly in expression between HUVECs exposed to severe heat treatment and untreated control cells (20 miRNAs were downregulated and miRNAs were 11 upregulated) (19). Only 1% of the human miRNA assemblage (31/3,100) exhibited differential expression following heat treatment, indicating that the regulatory activity of heat stress may be specific toward a subset of miRNAs in HUVECs.…”

Section: Introductionmentioning

confidence: 99%

“…Only 1% of the human miRNA assemblage (31/3,100) exhibited differential expression following heat treatment, indicating that the regulatory activity of heat stress may be specific toward a subset of miRNAs in HUVECs. Additionally, associations between miRNAs and genes have been previously evaluated on the basis of their differential expression levels, and according to interactions between miRNAs and genes reported in the Sanger miRNA database; these associations were used to build a miRNA-gene network that was employed to evaluate the regulatory effects of miRNAs on genes (19). Using this network model, miR-3613-3p was identified as a key miRNA that may serve a prominent role in the response to heat stress (19).…”

Section: Introductionmentioning

confidence: 99%

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Analysis of potential functional significance of microRNA‑3613‑3p in human umbilical vein endothelial cells affected by heat stress

et al. 2019

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Dysregulation of microRNA-3613-3p (miR-3613-3p) was previously reported in endothelial cells (ECs) during heat stress. The aim of the present study was to investigate the precise role of miR-3613-3p in heat stress. In the present study, potential gene targets of miR-3613-3p in heat-treated ECs were assessed, and the potential effects of miR-3613-3p were determined using Gene Ontology enrichment analysis. Kyoto Encyclopedia of Genes and Genomes pathway analysis was used to identify signaling pathways that may be affected by miR-3613-3p in heat-treated cells. Reverse transcription-quantitative PCR, western blotting and annexin V-FITC/propidium iodide staining were performed to detect miRNA expression, protein expression and apoptosis, respectively. Luciferase gene reporter assay was performed to evaluate the association between miR-3613-3p and mitogen-activated protein kinase kinase kinase 2 (MAP3K2). Bioinformatics analysis revealed 865 potential gene targets for miR-3613-3p and a series of functions and pathways in heat-treated ECs. ‘Negative regulation of apoptotic process’ was identified as a potential function of miR-3613-3p. In addition, functional analysis confirmed the downregulated expression levels of miR-3613-3p in ECs during heat stress, which was accompanied by an increase in apoptosis; restoration of miR-3613-3p expression inhibited apoptosis. MAP3K2 protein was demonstrated to be upregulated in heat-treated ECs, and overexpression of miR-3613-3p reduced MAP3K2 expression levels. Additionally, MAP3K2 was targeted by miR-3613-3p. These results indicated that miR-3613-3p may have complicated roles in ECs under heat stress. miR-3613-3p may serve an important role in the apoptosis of heat-treated ECs, and this effect may be partly achieved by targeting MAP3K2.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Analysis of potential functional significance of microRNA‑3613‑3p in human umbilical vein endothelial cells affected by heat stress

et al. 2019

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“…Inflammation-related gene expression in the brain can be regulated not only by transcription factors at the transcriptional level but also by miRNAs at the post-transcriptional level. Many miRNAs play an important role in heat-related disease (Roufayel et al, 2014; Liu et al, 2017). Given that miR-155 is upregulated by heat stress in peripheral blood mononuclear cells, as shown by deep sequence data analysis (Sengar et al, 2018), and participates in the proinflammatory responses (Faraoni et al, 2009), we hypothesized that miR-155 was deeply involved in regulating heat stress-induced microglial activation and inflammation.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-155 Promotes Heat Stress-Induced Inflammation via Targeting Liver X Receptor α in Microglia

Gong

Zhang

et al. 2019

Front. Cell. Neurosci.

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Background: The neuroinflammatory responses of microglial cells play an important role in the process of brain dysfunction caused by heat stroke. MicroRNAs are reportedly involved in a complex signaling network and have been identified as neuroinflammatory regulators. In this study, we determined the biological roles of microRNA-155 in the inflammatory responses in heat-stressed microglia and explored the underlying mechanisms.Methods: MicroRNA-155 mimic and inhibitor were used to separately upregulate or downregulate microRNA-155 expression. The activation state of BV-2 microglial cells (BV-2 cells) was assessed via immunoreactions using the microglial marker CD11b and CD68. Levels of induced interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were measured using real-time reverse transcription polymerase chain reaction (RT-PCR) and enzyme linked immunosorbent assays (ELISAs). The activation of nuclear factor kappa B (NF-κB) signaling proteins was evaluated by Western blotting for inhibitory kappa B alpha (IκBα) and NF-κB p65 phosphorylation and indirect immunofluorescence analysis using a p65 phosphorylation antibody. A luciferase reporter assay was used to verify liver X receptor α (LXRα) as a target gene of microRNA-155.Results: Heat stress significantly induced IL-1β, IL-6, and TNF-α release and increased the expression of CD11b and CD68. In addition, IκBα and NF-κB p65 phosphorylation were dramatically increased by heat stress, and microRNA-155 expression was also elevated. High expression of microRNA-155 in heat-stressed microglial cells was inversely correlated with LXRα expression. We then determined the role of microRNA-155 in the heat stress-induced inflammatory responses. The results revealed that by targeting LXRα, microRNA-155 enhanced NF-κB signaling activation and facilitated immune inflammation in heat stress-treated BV-2 cells.Conclusion: MicroRNA-155 promotes heat stress-induced inflammatory responses in microglia. The underlying mechanisms may include facilitating inflammatory factors expression by increasing NF-κB pathway activation via targeting LXRα.

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“…All experiments were performed in triplicate. Relative miRNA expression was calculated on the basis of the C T method where C T values of individual miRNA data were normalized to C T values of U6 snRNA as previously described [ 18 ].…”

Section: Methodsmentioning

confidence: 99%

Roles of miR-640 and Zinc Finger Protein 91 (ZFP91) in Angiopoietin-1-Induced In Vitro Angiogenesis

Harel

Sanchez‐Gonzalez

Echavarría

et al. 2020

Cells

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Angiopoietin-1 (Ang-1) is a ligand of Tie-2 receptors that promotes angiogenesis. It has been established that regulatory loops exist between angiogenic growth factors and distinct pro or anti-angiogenic miRNAs, but the nature and the roles of Ang-1-regulated miRNAs remain unclear. In this study, we assessed the role of miR-640 in Ang-1-induced angiogenesis in human umbilical vein endothelial cells (HUVECs). Exposure to Ang-1 (300 ng/mL) from 6 to 72 h significantly decreased expression of mature miR-640, a response that was mediated by Tie-2 receptors and was also observed in response to Ang-2, the vascular endothelial growth factor, and transforming growth factor β. Increasing miR-640 levels using a mimic inhibited Ang-1-induced cell migration and capillary-like tube formation whereas inhibition of miR-640 enhanced these responses. Pull down assays of biotinylated miR-640 revealed that miR-640 directly targets Zinc Finger Protein 91 (ZFP91), an atypical E3-ubiquitin ligase. Ang-1 exposure induced ZFP91 expression through down-regulation of miR-640. Silencing of ZFP91 significantly inhibited Ang-1-induced cell migration and tube formation. We conclude that Ang-1 upregulates ZFP91 expression through transcriptional down-regulation of miR-640 and that ZFP91 plays important roles in the promotion of Ang-1-induced endothelial cell migration and differentiation.

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Analysis of miRNA expression profiling in human umbilical vein endothelial cells affected by heat stress

Cited by 9 publications

References 82 publications

Analysis of potential functional significance of microRNA‑3613‑3p in human umbilical vein endothelial cells affected by heat stress

Analysis of potential functional significance of microRNA‑3613‑3p in human umbilical vein endothelial cells affected by heat stress

MicroRNA-155 Promotes Heat Stress-Induced Inflammation via Targeting Liver X Receptor α in Microglia

Roles of miR-640 and Zinc Finger Protein 91 (ZFP91) in Angiopoietin-1-Induced In Vitro Angiogenesis

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