LncRNA PVT1 induces apoptosis and inflammatory response of bronchial epithelial cells by regulating miR-30b-5p/BCL2L11 axis in COPD

Abstract Background Chronic obstructive pulmonary disease (COPD) is a serious health burden worldwide with high mortality. LncRNA plasmacytoma variant translocation 1 (PVT1) has been illustrated to serve as a biomarker for COPD progression. Nonetheless, its specific functions and mechanisms in COPD...

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Main Authors: Taoli Fu, Hui Tian, Hui Rong, Ping Ai, Xiaoping Li
Format: Article
Language:English
Published: BMC 2023-10-01
Series:Genes and Environment
Subjects:
Online Access:https://doi.org/10.1186/s41021-023-00283-4
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author Taoli Fu
Hui Tian
Hui Rong
Ping Ai
Xiaoping Li
author_facet Taoli Fu
Hui Tian
Hui Rong
Ping Ai
Xiaoping Li
author_sort Taoli Fu
collection DOAJ
description Abstract Background Chronic obstructive pulmonary disease (COPD) is a serious health burden worldwide with high mortality. LncRNA plasmacytoma variant translocation 1 (PVT1) has been illustrated to serve as a biomarker for COPD progression. Nonetheless, its specific functions and mechanisms in COPD are unclarified. Methods Cigarette smoke extract (CSE) was utilized to stimulate 16HBE cells, and cigarette smoke combining with lipopolysaccharide (LPS) was employed to induce COPD in rats. Western blotting and RT-qPCR were utilized for measuring protein and RNA levels. Flow cytometry was implemented for detecting cell apoptosis. Concentrations of inflammatory factors TNF-α and IFN-γ were examined using ELISA. Luciferase reporter assay was utilized for verifying the interaction between molecules. Hematoxylin–eosin staining was performed for histological analysis of rat lung tissues. Results PVT1 was highly expressed in CSE-stimulated 16HBE cells and the lungs of COPD rats. PVT1 depletion restored the viability, restrained apoptosis and hindered inflammatory cytokine production in 16HBE cells under CSE treatment and alleviated pathological damages in COPD rats. PVT1 bound to miR-30b-5p and miR-30b-5p targeted BCL2 like 11 (BCL2L11). Overexpressing BCL2L11 offset the above effects mediated by PVT1 in CSE-triggered 16HBE cells. Conclusion PVT1 enhances apoptosis and inflammation of 16HBE cells under CSE stimulation by modulating miR-30b-5p/BCL2L11 axis.
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spelling doaj.art-6a086549a8bd44989c01ea3bafae40b12023-11-26T14:15:03ZengBMCGenes and Environment1880-70622023-10-0145111010.1186/s41021-023-00283-4LncRNA PVT1 induces apoptosis and inflammatory response of bronchial epithelial cells by regulating miR-30b-5p/BCL2L11 axis in COPDTaoli Fu0Hui Tian1Hui Rong2Ping Ai3Xiaoping Li4Department of Geriatrics, Wuhan Hospital of Traditional Chinese MedicineDepartment of Pulmonology, Wuhan Hospital of Traditional Chinese MedicineDepartment of Geriatrics, Wuhan Hospital of Traditional Chinese MedicineDepartment of Surgery, Wuhan Hospital of Traditional Chinese MedicineDepartment of Orthopaedics, Wuhan Hospital of Traditional Chinese MedicineAbstract Background Chronic obstructive pulmonary disease (COPD) is a serious health burden worldwide with high mortality. LncRNA plasmacytoma variant translocation 1 (PVT1) has been illustrated to serve as a biomarker for COPD progression. Nonetheless, its specific functions and mechanisms in COPD are unclarified. Methods Cigarette smoke extract (CSE) was utilized to stimulate 16HBE cells, and cigarette smoke combining with lipopolysaccharide (LPS) was employed to induce COPD in rats. Western blotting and RT-qPCR were utilized for measuring protein and RNA levels. Flow cytometry was implemented for detecting cell apoptosis. Concentrations of inflammatory factors TNF-α and IFN-γ were examined using ELISA. Luciferase reporter assay was utilized for verifying the interaction between molecules. Hematoxylin–eosin staining was performed for histological analysis of rat lung tissues. Results PVT1 was highly expressed in CSE-stimulated 16HBE cells and the lungs of COPD rats. PVT1 depletion restored the viability, restrained apoptosis and hindered inflammatory cytokine production in 16HBE cells under CSE treatment and alleviated pathological damages in COPD rats. PVT1 bound to miR-30b-5p and miR-30b-5p targeted BCL2 like 11 (BCL2L11). Overexpressing BCL2L11 offset the above effects mediated by PVT1 in CSE-triggered 16HBE cells. Conclusion PVT1 enhances apoptosis and inflammation of 16HBE cells under CSE stimulation by modulating miR-30b-5p/BCL2L11 axis.https://doi.org/10.1186/s41021-023-00283-4COPDCigarette smokeInflammationApoptosisPVT1
spellingShingle Taoli Fu
Hui Tian
Hui Rong
Ping Ai
Xiaoping Li
LncRNA PVT1 induces apoptosis and inflammatory response of bronchial epithelial cells by regulating miR-30b-5p/BCL2L11 axis in COPD
Genes and Environment
COPD
Cigarette smoke
Inflammation
Apoptosis
PVT1
title LncRNA PVT1 induces apoptosis and inflammatory response of bronchial epithelial cells by regulating miR-30b-5p/BCL2L11 axis in COPD
title_full LncRNA PVT1 induces apoptosis and inflammatory response of bronchial epithelial cells by regulating miR-30b-5p/BCL2L11 axis in COPD
title_fullStr LncRNA PVT1 induces apoptosis and inflammatory response of bronchial epithelial cells by regulating miR-30b-5p/BCL2L11 axis in COPD
title_full_unstemmed LncRNA PVT1 induces apoptosis and inflammatory response of bronchial epithelial cells by regulating miR-30b-5p/BCL2L11 axis in COPD
title_short LncRNA PVT1 induces apoptosis and inflammatory response of bronchial epithelial cells by regulating miR-30b-5p/BCL2L11 axis in COPD
title_sort lncrna pvt1 induces apoptosis and inflammatory response of bronchial epithelial cells by regulating mir 30b 5p bcl2l11 axis in copd
topic COPD
Cigarette smoke
Inflammation
Apoptosis
PVT1
url https://doi.org/10.1186/s41021-023-00283-4
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