Dysregulated placental microRNAs in Early and Late onset Preeclampsia

Lykoudi, Alexandra; Kοlialexi, Aggeliki; Lambrou, George Ι.; Braoudaki, Maria; Siristatidis, Charalampos; Papaioanou, G; Tzetis, Maria; Mavrou, Ariadni; Παπαντωνίου, Ν.

doi:10.1016/j.placenta.2017.11.005

Cited by 51 publications

(40 citation statements)

References 41 publications

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“…However, there are few relevant studies on this miRNA. It has been revealed that dysregulated expression of miR-431 relates to the occurrence of preeclampsia [12], diffuse large B-cell lymphoma [13] and hepatocellular carcinoma [13, 14], among other conditions. However, the significance of miR-431 in lung development, including its regulation of pulmonary surfactant, has been poorly explored.…”

Section: Introductionmentioning

confidence: 99%

The role of miR-431-5p in regulating pulmonary surfactant expression in vitro

Sun

Chen

et al. 2019

Cell Mol Biol Lett

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Background Pulmonary surfactant is the complex mixture of lipid and protein that covers the alveolar surface. Pulmonary surfactant deficiency is one of the main causes of neonatal respiratory distress. Recent studies showed that miRNA plays an important role in lung development, but research into miR-431 regulation of pulmonary surfactant are sparse. In this study, we explored the regulatory role of miR-431-5p in the expression of pulmonary surfactant and identified its potential target gene, Smad4. Methods The bioinformatics tool TargetScan was used to predict the targets of miR-431. The expression of miR-431-5p was achieved via transfection of miR-431-5p mimics, an miR-431-5p inhibitor and corresponding negative control. The level of miR-431-5p was determined using quantitative real-time PCR. The CCK8 assay was conducted to confirm cell growth 12 h after transfection with miR-431-5p mimics, inhibitor or NC. Smad4 and surfactant-associated proteins in A549 were analyzed using western blot and quantitative real-time PCR. Results Smad4 was validated as a target of miR-431 in A549 cells. Overexpression of miR-431 accelerated A549 proliferation and inhibited A549 apoptosis. The mRNA and protein levels for the surfactant proteins (SP-A, SP-B, SP-C and SP-D) were found to be differentially expressed in A549 cells over- or under-expressing miR-431-5p. Conclusion Our results show that miR-431-5p is critical for pulmonary surfactant expression and that its regulation is closely related to the TGF-β/Smad4 pathway. These results will help us to study the pathophysiological mechanism of lung developmental diseases.

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Section: Introductionmentioning

confidence: 99%

The role of miR-431-5p in regulating pulmonary surfactant expression in vitro

Sun

Chen

et al. 2019

Cell Mol Biol Lett

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“…miRNAs are known to play a critical role in the pathogenesis of PCOS and pregnancy-related disorders 45 – 47 . Pathways such as adipocytokine signaling, oxytocin signaling, TNF signaling, progesterone-mediated oocyte maturation, estrogen signaling, MAPK, and FoxO signaling are known to be regulated by miRNAs and associated with pregnancy outcome 48 , 49 .…”

Section: Resultsmentioning

confidence: 99%

PCOSKBR2: a database of genes, diseases, pathways, and networks associated with polycystic ovary syndrome

Sharma

Barai

Kundu

et al. 2020

Sci Rep

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PolyCystic Ovary Syndrome KnowledgeBase (PCOSKBR2) is a manually curated database with information on 533 genes, 145 SNPs, 29 miRNAs, 1,150 pathways, and 1,237 diseases associated with PCOS. This data has been retrieved based on evidence gleaned by critically reviewing literature and related records available for PCOS in databases such as KEGG, DisGeNET, OMIM, GO, Reactome, STRING, and dbSNP. Since PCOS is associated with multiple genes and comorbidities, data mining algorithms for comorbidity prediction and identification of enriched pathways and hub genes are integrated in PCOSKBR2, making it an ideal research platform for PCOS. PCOSKBR2 is freely accessible at http://www.pcoskb.bicnirrh.res.in/.

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“…In the present study, miRNA deep sequencing in first trimester maternal plasma samples was performed to identify candidate biomarkers associated with the subsequent development of LOPE and provide useful insights regarding pathways associated with the initiation and the development of this pregnancy related complication. In a previous study, we documented differential expression of placental and circulating miRNAs in PE highlighting a significant role of this epigenetic mechanism in the pathogenesis of the complication (18). That study was performed in placenta samples, thus limiting its potential use in prenatal screening.…”

Section: Discussionmentioning

confidence: 99%