Effects of Brain-Derived Neurotrophic Factor on MicroRNA Expression Profile in Human Endothelial Progenitor Cells

He, Tongrong; Sun, Ruohan; Li, Ying; Katušić, Zvonimir S.

doi:10.1177/0963689718761658

Cited by 13 publications

(10 citation statements)

References 22 publications

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“…A decrease in miR-636 is also involved in the recovery from heart failure due to dilated cardiomyopathy (25). Furthermore, in human endothelial cell progenitors, brain-derived neurotrophic factor is able to increase miR-636 expression (34). Interestingly, miR-636 manifests other biological effects; for instance, circulating miR-636 is involved in the elimination of hepatitis C virus (HCV) and also in liver regeneration.…”

Section: Discussionmentioning

confidence: 99%

miR-636: A Newly-Identified Actor for the Regulation of Pulmonary Inflammation in Cystic Fibrosis

et al. 2019

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Cystic fibrosis (CF) results from deficient CF transmembrane conductance regulator (CFTR) protein activity leading to defective epithelial ion transport. Pulmonary degradation due to excessive inflammation is the main cause of morbidity and mortality in CF patients. By analysing miRNAs (small RNAseq) in human primary air-liquid interface cell cultures, we measured the overexpression of miR-636 in CF patients compared to non-CF controls. We validated these results in explant biopsies and determined that the mechanism underlying miR-636 overexpression is linked to inflammation. To identify specific targets, we used bioinformatics analysis to predict whether miR-636 targets the 3′-UTR mRNA regions of IL1R1 and RANK (two pro-inflammatory cytokine receptors), IKBKB (a major protein in the NF-κB pathway), and FAM13A (a modifier gene of CF lung phenotype implicated in epithelial remodelling). Using bronchial epithelial cells from CF patients to conduct a functional analysis, we showed a direct interaction between miR-636 and IL1R1, RANK, and IKBKB, but not with FAM13A. These interactions led to a decrease in IL1R1 and IKKβ protein expression levels, while we observed an increase in RANK protein expression levels following the overexpression of miR-636. Moreover, NF-κB activity and IL-8 and IL-6 secretions decreased following the transfection of miR-636 mimics in CF cells. Similar but opposite effects were found after transfection with an antagomiR-636 in the same cells. Furthermore, we demonstrated that miR-636 was not regulated by Pseudomonas aeruginosa in our model. We went on to show that miR-636 is raised in the blood neutrophils, but not in the plasma, of CF patients and may have potential as a novel biomarker. Collectively, our findings reveal a novel actor for the regulation of inflammation in CF, miR-636, which is able to reduce constitutive NF-κB pathway activation when it is overexpressed.

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Section: Discussionmentioning

confidence: 99%

miR-636: A Newly-Identified Actor for the Regulation of Pulmonary Inflammation in Cystic Fibrosis

et al. 2019

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“…Considering this report and our results, a higher level of miRNA-4669 might contribute to the protection of vascular disease such as IS and arterial occlusive disease. Furthermore, a previous study reported the effect of BDNF on regenerative function of endothelial progenitor cells (EPCs), depending on the expression changes of miRNAs [27]. The treatment of BDNF could increase the expression of miRNA-4669 in EPCs [27].…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, a previous study reported the effect of BDNF on regenerative function of endothelial progenitor cells (EPCs), depending on the expression changes of miRNAs [27]. The treatment of BDNF could increase the expression of miRNA-4669 in EPCs [27]. BDNF production was increased on the surface of blood vessels with damaged endothelium, exerting beneficial effects on regenerative function of EPCs [28].…”

Section: Discussionmentioning

confidence: 99%

Association between MicroRNA-4669 Polymorphism and Ischemic Stroke in a Korean Population

et al. 2019

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Recent studies have explored the association between single-nucleotide polymorphisms (SNPs) in microRNAs (miRNAs) and ischemic stroke (IS). In particular, the associations of rs2910164 (miRNA-146A), rs11614913 (miRNA-196A2), and rs3746444 (miRNA-499A) were intensively studied in IS. In this study, we investigated the associations between SNPs in miRNAs and IS including rs2910164, rs11614913, and rs3746444 in a Korean population. For a pilot study, we selected 19 SNPs in pre-miRNA region (including mature miRNA region) and genotyped in 140 IS patients and 240 control subjects using the Fluidigm Dynamic Array. Our pilot study showed a weak association of rs79402775 in miRNA-933 (p = 0.044) and a relatively strong association of rs35196866 in miRNA-4669 (p = 0.016) with IS. From the pilot study, we selected rs79402775, rs35196866, and rs7202008 (miRNA-2117; p = 0.055) as candidate miRNA SNPs on IS and further genotyped these SNPs in 264 IS patients and 455 control subjects using direct sequencing. In addition, we further analyzed the associations of rs2910164, rs11614913, and rs3746444 that have been intensively studied in previous studies. In the further analysis, we found the significant association between rs35196866 and IS (p = 0.0014 in additive model and p = 0.00015 in dominant model; p = 0.00037 in allele frequency analysis). However, the association between rs2910164, rs11614913, rs3746444, rs79402775, and rs7202008 and IS was not shown. These results suggest that miRNA-4669 may be involved in the susceptibility of IS.

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Section: Introductionmentioning

confidence: 99%

“…MiR-1539 is 21 nucleotides long, to date, a few articles have been published ( 18 – 20 ). He et al observed that miR-1539 was inhibited by brain-derived neurotrophic factor, which stimulated angiogenesis and promoted endothelial cell survival ( 18 ). Ayaz et al indicated that miR-1539 overexpression was putatively involved in the pathological process of senile macular degeneration, with oxidative stress ( 19 ), whereas Veija et al reported that miR-1539 was associated with polyomavirus-positive Merkel cell carcinoma ( 20 ).…”

Section: Introductionmentioning

confidence: 99%

MiR-1539 and Its Potential Role as a Novel Biomarker for Colorectal Cancer

Cui

Ding

et al. 2021

Front. Oncol.

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PurposeWe investigated microRNA (miR) 1539 as a potential biomarker for predicting the risk and pathobiological behavior of colorectal cancer (CRC).MethodsOur strategy consisted of analyzing 100 serum samples from 51 CRC patients, 49 healthy controls (HCs), and another 56 CRC tissue and matched normal adjacent to tumor (NAT) samples. The relative expression levels of miR-1539 in exosomes, serum and tissues were detected and compared in the different groups, using reverse transcription-polymerase chain reaction (RT-qPCR). The diagnostic value and potential function of miR-1539 were investigated using clinicopathological data combined with bioinformatics analysis.ResultsMiR-1539 expression was significantly up-regulated in exosomes (p = 0.003) and cancer tissue (p < 0.001) from CRC patients. MiR-1539 expression levels in serum varied according to different tumor sites (right-sided vs. left-sided, p = 0.047; left-side CRC vs. HCs, p = 0.031). In terms of diagnostic efficacy, miR-1539 expression in exosomes may help distinguish CRC cases from HCs with a sensitivity of 92.2%, and miR-1539 expression in serum may improve the specificity to 96.6% for left-sided CRC diagnosis. When combined with clinicopathological data, serum miR-1539 levels were positively associated with vascular endothelial growth factor (VEGF) expression (p = 0.028), whilst levels in CRC tissue were positively associated with increased Ki-67 levels (p = 0.035). Poorer pathologic differentiation was potentially related to an increased tendency of miR-1539 expression in CRC tissue (p = 0.071). Based on our bioinformatics analysis, miR-1539 may have a significant mechanistic influence on CRC genesis and progression.ConclusionsCirculating or tissue based miR-1539 may be used as a novel potential biomarker for CRC screening, and a predictor of poor clinicopathological behavior in tumors.

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Effects of Brain-Derived Neurotrophic Factor on MicroRNA Expression Profile in Human Endothelial Progenitor Cells

Cited by 13 publications

References 22 publications

miR-636: A Newly-Identified Actor for the Regulation of Pulmonary Inflammation in Cystic Fibrosis

miR-636: A Newly-Identified Actor for the Regulation of Pulmonary Inflammation in Cystic Fibrosis

Association between MicroRNA-4669 Polymorphism and Ischemic Stroke in a Korean Population

MiR-1539 and Its Potential Role as a Novel Biomarker for Colorectal Cancer

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