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논문 기본 정보

자료유형
학술저널
저자정보
Xiangying Wang (Hangzhou Children’s Hospital) Ruju Xu (Hangzhou Children’s Hospital) Di Chi (Hangzhou Children’s Hospital) Chufeng Dai (Hangzhou Children’s Hospital) Meiling Sheng (Hangzhou Children’s Hospital)
저널정보
연세대학교 의과대학 Yonsei Medical Journal Yonsei Medical Journal 제62권 제9호
발행연도
2021.9
수록면
858 - 867 (10page)
DOI
10.3349/ymj.2021.62.9.858

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Purpose: Asthma is a serious inflammatory disease of the respiratory system in which airway smooth muscle cells (ASMCs) playa key role. This study aimed to investigate the expression of SLC26A2 in human ASMCs (HASMCs) and the regulatory mechanismof SLC26A2 in the proliferation and inflammatory factor production of HASMCs. Materials and Methods: We obtained the asthma-associated differential mRNA SLC26A2 by bioinformatics analysis in childhoodacute asthma samples. To investigate its role in airway inflammation and airway remodeling, we treated HASMCs with plateletderivedgrowth factor (PDGF) in an in vitro model and determined SLC26A2 expression in cells using western blotting. Cell proliferationwas detected by MTT and EdU assays, and cell contractile phenotype marker proteins were measured. Cell migrationand production of inflammatory factors were determined by Transwell and ELISA assays. Additionally, the upstream regulatorymiRNA and LncRNA of SLC26A2 were identified by bioinformatics, luciferase reporter gene, and RIP analyses. Results: SLC26A2 was significantly upregulated in bioinformatics analysis of pediatric asthma-related sample. PDGF treatmentup-regulated SLC26A2 expression in HASMCs, whereas the knockdown of SLC26A2 inhibited PDGF-stimulated proliferation,migration, and production of inflammatory factors, and enhanced the expression of cell contractile phenotype marker proteinsin HASMCs. Luciferase reporter and RIP experiments validated that NEAT1 targeted miR-9-5p to regulate SLC26A2, thereby influencingthe biological function of PDGF-induced HASMCs. Conclusion: These findings indicate that NEAT1-mediated miR-9-5p targeting of SLC26A2 inhibits the PDGF-induced proliferationand production of inflammatory factors in HASMCs. These findings highlight potential therapeutic targets for asthma andairway inflammation.

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