1. MALAT1 binds to miR-188–3p to regulate ALOX5 activity in the lung inflammatory response of neonatal bronchopulmonary dysplasia.
- Author
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Feng, Dan-dan, Chen, Jia-he, Chen, Yu-fei, Cao, Qian, Li, Bing-jie, Chen, Xiao-qing, Jin, Rui, and Zhou, Guo-ping
- Subjects
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BRONCHOPULMONARY dysplasia , *MONONUCLEAR leukocytes , *DYSPLASIA , *INFLAMMATION , *GENE expression , *INHIBITION of cellular proliferation - Abstract
Bronchopulmonary dysplasia (BPD) causes high morbidity and mortality in infants, but no effective preventive or therapeutic agents have been developed to combat BPD. In this study, we assessed the expression of MALAT1 and ALOX5 in peripheral blood mononuclear cells from BPD neonates, hyperoxia-induced rat models and lung epithelial cell lines. Interestingly, we found upregulated expression of MALAT1 and ALOX5 in the experimental groups, along with upregulated expression of proinflammatory cytokines. According to bioinformatics prediction, MALAT1 and ALOX5 simultaneously bind to miR-188–3p, which was downregulated in the experimental groups above. Silencing MALAT1 or ALOX5 and overexpressing miR-188–3p inhibited apoptosis and promoted the proliferation of hyperoxia-treated A549 cells. Suppressing MALAT1 or overexpressing miR-188–3p increased the expression levels of miR-188–3p but decreased the expression levels of ALOX5. Moreover, RNA immunoprecipitation (RIP) and luciferase assays showed that MALAT1 directly targeted miR-188–3p to regulate ALOX5 expression in BPD neonates. Collectively, our study demonstrates that MALAT1 regulates ALOX5 expression by binding to miR-188–3p, providing novel insights into potential therapeutics for BPD treatment. • MALAT1 and ALOX5 are highly expressed in BPD. • Silencing MALAT1 or ALOX5 promotes cell proliferation and inhibits cell apoptosis. • MALAT1 and ALOX5 directly targeted by miR-188–3p in hyperoxia-induced injury in A549 cells. • MALAT1/miR-188–3p/ALOX5 affects lung inflammatory response of BPD. [ABSTRACT FROM AUTHOR]
- Published
- 2023
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