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LncRNA PVT1 exacerbates the inflammation and cell-barrier injury during asthma by regulating miR-149
Lianmei Ma1, Qian Zhang2, Jinping Hao2
1Department of Pediatrics, Binzhou Medical University Hospital, Binzhou, Shandong, China.
Insights
Long non-coding RNA PVT1 promotes asthma by increasing airway inflammation. Targeting PVT1 and its interaction with miR-149 may offer new therapeutic strategies for childhood asthma.
Area of Science:
- Molecular Biology
- Immunology
- Respiratory Medicine
Background:
- Asthma is a common childhood respiratory disease involving airway inflammation and hyperresponsiveness.
- Long non-coding RNAs (lncRNAs) are implicated in various diseases, but their role in asthma remains underexplored.
- This study investigates the role of lncRNA PVT1 in promoting airway inflammation in asthma.
Purpose of the Study:
- To elucidate the role of lncRNA PVT1 in the pathogenesis of asthma.
- To investigate the underlying mechanisms by which PVT1 influences airway inflammation.
- To explore the potential of PVT1 as a therapeutic target for asthma.
Main Methods:
- Human small airway epithelial cells (HSAECs) were manipulated for PVT1 overexpression or knockdown and treated with platelet activating factor (PAF) to model asthma in vitro.
- Inflammatory markers (PGE2, IL-1β, IL-6, TNF-α) and signaling proteins (PKC, MyD88, NF-ĸB) were quantified.
- Cell permeability assays and luciferase reporter gene assays were performed to assess cell barrier function and PVT1-miR-149 interaction.
Main Results:
- Knockdown of PVT1 reduced PAF-induced inflammatory responses and protected cell barrier integrity.
- PVT1 overexpression exacerbated asthma-like pathological changes in HSAECs.
- PVT1 directly targets miR-149, and miR-149 overexpression reversed the pro-inflammatory effects of PVT1.
Conclusions:
- lncRNA PVT1 plays a significant role in promoting airway inflammation in asthma.
- The PVT1/miR-149 axis is a key mechanism in asthma pathogenesis.
- PVT1 emerges as a promising novel therapeutic target for asthma treatment.
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.
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