4.2 Article

lncRNA-NEAT1 Sponges miR-128 to Promote Inflammatory Reaction and Phenotypic Transformation of Airway Smooth Muscle Cells

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HINDAWI LTD
DOI: 10.1155/2022/7499911

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This study investigated the relationship between pediatric asthma and lncRNA-NEAT1 and miR-128. The results showed that lncRNA-NEAT1 can enhance the inflammatory reaction and phenotypic transformation of airway smooth muscle cells, thereby exacerbating the occurrence and development of childhood bronchial asthma.
Objective. Pediatric asthma is still a health threat to the children. Long noncoding RNA-NEAT1 (lncRNA-NEAT1) was reported to be positively correlated with the severity of asthma. We aimed to study the effects and mechanism of lncRNA-NEAT1on inflammatory reaction and phenotypic transformation of airway smooth muscle cells (ASMCs) in the bronchial asthma. Method. The degree of lncRNA-NEAT1 and miR-128 mRNA in children with bronchial asthma and healthy individuals was tested by qRT-PCR. After the inflammatory reaction and phenotypic transformation of PDGF-BB-induced ASMCs, the expression of lncRNA-NEAT1 or miR-128 in the AMSC was disturbed in the AMSC. Subsequently, the expression of lncRNA-NEAT1 and miR-128 was detected by the way of qRT-PCR, and western blot was applied to measure the expression of MMP-2, MMP-9, alpha-SMA, calponin, NF-kappa B, and so on in the cells. The content of TNF-alpha, IL-1 beta, IL-6, and IL-8 in the cell culture supernatant was checked by ELISA. MTT, Transwell, and flow cytometry were used to detect cell proliferation, migration, and apoptosis. Further, the targeting relations between lncRNA-NEAT1 and miR-128 were evaluated by the dual-luciferase reporter assay. Result. In the sputum of children with bronchial asthma, lncRNA-NEAT1 was significantly upregulated while miR-128 was rapidly downregulated. Besides, lncRNA-NEAT1 and miR-128 were competitively combined and, for their expression, negatively correlated. Conclusion. lncRNA-NEAT1 sponges miR-128 to boost PDGF-BB-induced inflammatory reaction and phenotypic transformation of ASMCs to aggravate the occurrence and development of childhood bronchial asthma.

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