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논문 기본 정보

자료유형
학술저널
저자정보
Rui Zhang (Hubei University of Medicine) Lina Chen (Hubei University of Medicine) Fei Huang (Hubei University of Medicine) Xiaorong Wang (Hubei University of Medicine) Cuihong Li (Hubei University of Medicine)
저널정보
한국유전학회 Genes & Genomics Genes & Genomics Vol.43 No.7
발행연도
2021.1
수록면
815 - 827 (13page)

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Background Many long non-coding RNAs (lncRNAs) have been suggested to play critical roles in acute lung injury (ALI) pathogenesis, including lncRNA nuclear enriched abundant transcript 1 (NEAT1). Objective We aimed to further elucidate the functions and molecular mechanism of NEAT1 in ALI. Methods Human pulmonary alveolar epithelial cells (HPAEpiCs) stimulated by lipopolysaccharide (LPS) were served as a cellular model of ALI. Cell viability and cell apoptosis were determined by cell counting kit-8 (CCK-8) assay and flow cytometry, respectively. The expression of NEAT1, microRNA-424-5p (miR-424-5p), and mitogen-activated protein kinase 14 (MAPK14) was measured by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot analysis. Caspase activity was determined by caspase activity kit. The inflammatory responses were evaluated using enzyme-linked immunosorbent assay (ELISA). The oxidative stress factors were analyzed by corresponding kits. Results NEAT1 was upregulated in LPS-stimulated HPAEpiCs. NEAT1 knockdown weakened LPS-induced injury by inhibiting apoptosis, inflammation and oxidative stress in HPAEpiCs. Moreover, miR-424-5p was a direct target of NEAT1, and its knockdown reversed the effects caused by NEAT1 knockdown in LPS-induced HPAEpiCs. Furthermore, MAPK14 was a downstream target of miR-424-5p, and its overexpression attenuated the effects of miR-424-5p on reduction of LPS-induced injury in HPAEpiCs. Besides, NEAT1 acted as a sponge of miR-424-5p to regulate MAPK14 expression. Conclusion NEAT1 knockdown alleviated LPS-induced injury of HPAEpiCs by regulating miR-424-5p/MAPK14 axis, which provided a potential therapeutic target for the treatment of ALI.

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