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LncRNA PVT1 exacerbates the inflammation and cell‐barrier injury during asthma by regulating miR‐149
Author(s) -
Ma Lianmei,
Zhang Qian,
Hao Jinping,
Wang Jianqiang,
Wang Chunjian
Publication year - 2020
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.22563
Subject(s) - pvt1 , inflammation , immunology , gene knockdown , tumor necrosis factor alpha , cancer research , asthma , cytokine , biology , medicine , downregulation and upregulation , cell culture , long non coding rna , gene , biochemistry , genetics
Background Asthma is a prevailing respiratory disease among children, characterized by allergic airway inflammation, airway remodeling, and airway hyperresponsiveness. Although it is well‐known that long non‐coding RNAs (lncRNAs) are linked to a variety of human diseases and well‐documented, very few studies explore its role in asthma. In this study, we investigate the effects of lncRNA PVT1 on the promotion of airway inflammation and its associated mechanisms. Methods and Materials Human small airway epithelial cells (HSAECs) with PVT1 overexpressed or knocked down were constructed, and platelet activating factor (PAF) was used to treat HSAECs to mimic the pathological process of asthma in vitro. The expressions of prostaglandin E2 (PGE2), interleukin‐1β (IL‐1β), IL‐6, and tumor necrosis factor‐α (TNF‐α) were measured by enzyme‐linked immunosorbent assay (ELISA). The expressions of PKC, MyD88, and NF‐ĸB were measured by Western blot. Monolayer permeability of HSAECs was also compared within different groups. Luciferase reporter gene assay was employed to detect the targeting relationship between PVT1 and miR‐149. Results The knockdown of PVT1 attenuated the levels of inflammatory factors induced by PAF and destruction of cell‐barrier function. The overexpression of PVT1 facilitated the pathological development. Additionally, miR‐149 was identified as a target microRNA of PVT1, and the overexpression of miR‐149 could reverse the effects of PVT1 on PAF‐induced HSAECs. Conclusion These findings suggest that PVT1 may represent a novel potential target for treatment of asthma.