ArticleMolecular genetics & genomic medicine2019
MiR-182-5p enhances in vitro neutrophil infiltration in Kawasaki disease.
Article in Molecular genetics & genomic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- MicroRNAs in Kawasaki disease: An update on diagnosis, therapy and monitoring.Frontiers in immunology · 2022Pooled it
- Advances in understanding Kawasaki disease-related immuno-inflammatory response and vascular endothelial dysfunction.Pediatric investigation · 2022Review
- iTRAQ Proteomics Identified the Potential Biomarkers of Coronary Artery Lesion in Kawasaki Disease and In Vitro Studies Demonstrated That S100A4 Treatment Made HCAECs More Susceptible to Neutrophil Infiltration.International journal of molecular sciences · 2022Article
- Comparable bidirectional neutrophil immune dysregulation between Kawasaki disease and severe COVID-19.Frontiers in immunology · 2022Article
- Pulmonary EV miRNA profiles identify disease and distinct inflammatory endotypes in COPD.Frontiers in medicine · 2022Article
- Insights Into Coronary Artery Lesions in Kawasaki Disease.Frontiers in pediatrics · 2020Review
- MiR-182-5p enhances in vitro neutrophil infiltration in Kawasaki disease.Molecular genetics & genomic medicine · 2019Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundKawasaki disease (KD) patients could develop coronary artery lesion (CAL) which threatens children's life. A previous study identified KD biomarker miRNAs that could discriminate KD patients from febrile non-KD patients. We wonder whether these KD prediction biomarkers could be further applied to predict CAL formation in KD patients.
methodsTo examine this hypothesis, we conducted a meta-analysis, miRNA mimic transfection, in vitro cell model and microarray assays.
resultsWe first showed that miR-182-5p and miR-183-5p kept higher levels in the KD patients with CAL than those without CAL (p < .05). Further machine learning alignment confirmed that CAL formation could be predicted, with an auROC value of 0.86. We further treated neutrophil cells with miR-182-5p mimic, followed by in vitro transendotherial migration assay. As a result, miR-182-5p overexpression significantly (p < .05) enhanced neutrophil cells to infiltrate the endothelial layer composed of human coronary artery endothelium cells. Further microarray assay and pathway enrichment analysis showed that the genes activated with miR-182-5p overexpression were significantly enriched in the leukocyte transendothelial migration pathway (kegg_pathway_194, p < .05).
conclusionTherefore, our study suggested that miR-182-5p enhanced in vitro leukocyte infiltration by activating the leukocyte transendothelial migration pathway in CAL formation in KD.
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