miR-379 Inhibits Cell Proliferation, Invasion, and Migration of Vascular Smooth Muscle Cells by Targeting Insulin-Like Factor-1

Li, Kai; Wang, Yong; Zhang, Anji; Liu, Baixue; Li, Jia

doi:10.3349/ymj.2017.58.1.234

Cited by 31 publications

(23 citation statements)

References 28 publications

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“…Fifteen DE miRNAs were identified on the seventh day in the tracheal tissue (as shown in Supplementary Table 6 ). At this stage, miRNAs may restore the state of the organism to normal; these included miR-379, which inhibited cell proliferation invasion ( Li et al, 2017 ), anti-inflammatory-related miR-127 ( Zhang et al, 2017 ), and apoptosis-related miR-410 ( Palumbo et al, 2016 ; Deng H. et al, 2017 ).…”

Section: Resultsmentioning

confidence: 99%

Integrated Lung and Tracheal mRNA-Seq and miRNA-Seq Analysis of Dogs with an Avian-Like H5N1 Canine Influenza Virus Infection

Luo

et al. 2018

Front. Microbiol.

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Avian-like H5N1 canine influenza virus (CIV) causes severe respiratory infections in dogs. However, the mechanism underlying H5N1 CIV infection in dogs is unknown. The present study aimed to identify differentially expressed miRNAs and mRNAs in the lungs and trachea in H5N1 CIV-infected dogs through a next-generation sequencing-based method. Eighteen 40-day-old beagles were inoculated intranasally with CIV, A/canine/01/Guangdong/2013 (H5N1) at a tissue culture infectious dose 50 (TCID50) of 106, and lung and tracheal tissues were harvested at 3 and 7 d post-inoculation. The tissues were processed for miRNA and mRNA analysis. By means of miRNA-gene expression integrative negative analysis, we found miRNA–mRNA pairs. Lung and trachea tissues showed 138 and 135 negative miRNA–mRNA pairs, respectively. One hundred and twenty negative miRNA–mRNA pairs were found between the different tissues. In particular, pathways including the influenza A pathway, chemokine signaling pathways, and the PI3K-Akt signaling pathway were significantly enriched in all groups in responses to virus infection. Furthermore, dysregulation of miRNA and mRNA expression was observed in the respiratory tract of H5N1 CIV-infected dogs and notably, TLR4 (miR-146), NF-κB (miR-34c) and CCL5 (miR-335), CCL10 (miR-8908-5p), and GNGT2 (miR-122) were found to play important roles in regulating pathways that resist virus infection. To our knowledge, the present study is the first to analyze miRNA and mRNA expression in H5N1 CIV-infected dogs; furthermore, the present findings provide insights into the molecular mechanisms underlying influenza virus infection.

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Section: Resultsmentioning

confidence: 99%

Integrated Lung and Tracheal mRNA-Seq and miRNA-Seq Analysis of Dogs with an Avian-Like H5N1 Canine Influenza Virus Infection

Luo

et al. 2018

Front. Microbiol.

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“…Wang et al reported that miR-422a was downregulated in glioma tissues and was negatively correlated with the expression levels of IGF1/IGF1R [ 39 ]. Li et al demonstrated that miR-379 plays an important role in regulating vascular smooth muscle cells proliferation, invasion, and migration by targeting IGF-1 [ 40 ]. Budzinska et al found that miR-96, miR-145, and expression were increased while IGF-1R was decreased in peripheral blood mononuclear cells of aging humans.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Hypoxia on the Expression of miR-646/IGF-1 Signaling in Human Periodontal Ligament Cells (hPDLCs)

et al. 2018

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BackgroundThis study aims to investigate the role of miR-646 in hypoxia conditions in human periodontal ligament cells (hPDLCs), exploring the effect of hypoxia on hPDLCs proliferation and apoptosis. In addition, this study aimed to explore the potential mechanism of miR-646/IGF-1 signaling in hPDLCs in hypoxia conditions.Material/MethodshPDLCs (fifth passage) cultured by the tissue culture method were randomly assigned to the severe hypoxia (1% O2) group, the slight hypoxia (5% O2) group or the control (21% O2) group. Then reverse transcription quantitative real-time polymerase chain reaction and western blot analysis were used to detect the mRNA and protein expression of miR-646 and IGF-1. hPDLCs infected with lentivirus (LV)-pre-miR-646 or LV-anti-mR-646, and negative controls were cultured. MTT assay, caspase-3 ELISA assay, and wound healing assay were performed to evaluate how miR-646 was influenced by hypoxia. In addition, the relationship between miR-646 and IGF-1 was explored.ResultsThe expression of miR-646 was downregulated and IGF-1 was upregulated in hypoxia conditions. MiR-646 was able to suppress hPDLCs proliferation and promote apoptosis in hypoxia conditions. The mRNA and protein expressions of IGF-1 were downregulated when miR-646 was overexpressed and upregulated when miR-646 was downregulated.ConclusionsThis finding identified a significant role of miR-646 in hPDLCs in suppressing cell proliferation and promoting apoptosis by inversely regulating IGF-1 expression. Meanwhile, the regulation of hPDLCs in hypoxia may be through the miR-646/IGF-1 signaling pathway, probably serving as a promising therapeutic target for periodontal diseases.

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“…[ 11 ]. Previously, we have demonstrated that miR-379 was down-regulated after PDGF-bb treatment, and miR-379 was found to suppress the VSMCs proliferation, invasion and migration via targeting insulin-like factor-1 [ 12 ]. In addition, lots of miRNAs have been shown to have a regulatory role for VSMCs proliferation and migration.…”

Section: Introductionmentioning

confidence: 99%

MiR-137 inhibited cell proliferation and migration of vascular smooth muscle cells via targeting IGFBP-5 and modulating the mTOR/STAT3 signaling

Jin

Huang

et al. 2017

PLoS ONE

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Abnormal proliferation of vascular smooth muscle cells (VSMCs) contributes to the development of cardiovascular diseases. Studies have shown the great impact of microRNAs (miRNAs) on the cell proliferation of VSMCs. This study examined the effects of miR-137 on the cell proliferation and migration of VSMCs and also explored the underlying molecular mechanisms. The mRNA and protein expression levels were determined by qRT-PCR and western blot assays, respectively. The CCK-8 assay, wound healing assay and transwell migration assay were performed to measure cell proliferation and migration of VSMCs. The miR-137-targeted 3’untranslated region of insulin-like growth factor-binding protein-5 (IGFBP-5) was confirmed by luciferase reporter assay. Platelet-derived growth factor-bb (PDGF-bb) treatment enhanced cell proliferation and suppressed the expression of miR-137 in VSMCs. The gain-of-function and loss-of-function assays showed that overexpression of miR-137 suppressed the cell proliferation and migration, and also inhibited the expression of matrix genes of VSMCs; down-regulation of miR-137 had the opposite effects on VSMCs. Bioinformatics analysis and luciferase report assay results showed that IGFBP-5 was a direct target of miR-137, and miR-137 overexpression suppressed the IGFBP-5 expression and down-regulation of miR-137 increased the IGFBP-5 expression in VSMCs. PDGF-bb treatment also increased the IGFBP-5 mRNA expression. In addition, enforced expression of IGFBP-5 reversed the inhibitory effects of miR-137 on cell proliferation and migration of VSMCs. More importantly, overexpression of miR-137 also suppressed the activity of mTOR/STAT3 signaling in VSMCs. Taken together, the results suggest that miR-137 may suppress cell proliferation and migration of VSMCs via targeting IGFBP-5 and modulating mTOR/STAT3 signaling pathway.

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miR-379 Inhibits Cell Proliferation, Invasion, and Migration of Vascular Smooth Muscle Cells by Targeting Insulin-Like Factor-1

Cited by 31 publications

References 28 publications

Integrated Lung and Tracheal mRNA-Seq and miRNA-Seq Analysis of Dogs with an Avian-Like H5N1 Canine Influenza Virus Infection

Integrated Lung and Tracheal mRNA-Seq and miRNA-Seq Analysis of Dogs with an Avian-Like H5N1 Canine Influenza Virus Infection

Evaluation of Hypoxia on the Expression of miR-646/IGF-1 Signaling in Human Periodontal Ligament Cells (hPDLCs)

MiR-137 inhibited cell proliferation and migration of vascular smooth muscle cells via targeting IGFBP-5 and modulating the mTOR/STAT3 signaling

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