Jie Feng1,
Jingjing Tang1,
Pingping Liu2,
Xiaolan Zhang2
1Department of Pediatrics, The People's Hospital of Fenghua Ningbo, Ningbo City, Zhejiang Province 315500;
2Department of Pediatrics, Jiangning Hospital Affiliated to Nanjing Medical University, Nanjing City, Jiangsu Province 211100, China.
For correspondence:- Xiaolan Zhang
Email: xiaolanzhang188@126.com Tel:+862552281848
Accepted: 26 February 2021
Published: 31 March 2021
Citation:
Feng J, Tang J, Liu P, Zhang X.
MiR-483-3p exacerbates pediatric pneumonia by suppressing IGF1 expression in alveolar macrophage. Trop J Pharm Res 2021; 20(3):483-489
doi:
10.4314/tjpr.v20i3.6
© 2021 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..
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.
Keywords: MiR-483-3p, Insulin-like growth factor (IGF1), TNBC, Alveolar macrophage, Pediatric pneumonia