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Published:
Jan 17, 2022DOI:
10.4314/tjpr.v20i3.6Keywords:
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Main Article Content
MiR-483-3p exacerbates pediatric pneumonia by suppressing IGF1 expression in alveolar macrophage
Abstract
Purpose: To investigate the action of miR-483-3p in pediatric pneumonia and identify potential biomarkers.
Methods: Bronchoalveolar lavage was collected from 38 pneumonia patients and 25 healthy children. The expression of miR-483-3p in the lavage was determined using qRT-PCR. Alveolar macrophages collected from lavage of healthy children were cultured and used for functional assays. Transwell assay was conducted to evaluate macrophage cell migration. Cell viability and apoptosis were evaluated in lipopolysaccharide (LPS)-induced human pulmonary alveolar epithelial cells (HPAEpiCs) by CCK8 (cell counting kit - 8) or flow cytometry, respectively.
Results: MiR-483-3p was significantly elevated in bronchoalveolar lavage of pneumonia patients, when compared to healthy children (p < 0.001). MiR-483-3p, which targets insulin-like growth factor 1 (IGF1), decreased the mRNA and protein expression of IGF1 in alveolar macrophages collected from the lavage of healthy children. MiR-483-3p reduced motility of macrophages. IGF1 counteracted the LPS- induced decrease in cell viability and the increase in apoptosis of HPAEpiCs. Conditioned medium from macrophages transfected with miR-483-3p inhibitor increased cell viability and reduced cellular apoptosis of LPS-induced HPAEpiCs. However, conditioned medium from macrophages transfected with miR-483-3p mimics decreased cell viability and increased apoptosis.
Conclusion: MiR-483-3p negatively regulates IGF1 to promote progression of pediatric pneumonia, providing a potential therapeutic target in pediatric pneumonia.
