Long non‐coding RNA PVT1, a novel biomarker for chronic obstructive pulmonary disease progression surveillance and acute exacerbation prediction potentially through interaction with microRNA‐146a

Abstract

Objective This study aimed to investigate the abilities of long non‐coding RNA PVT1 (lnc‐PVT1) and microRNA‐146a (miR‐146a) in predicting chronic obstructive pulmonary disease (COPD) susceptibility and acute exacerbation risk, moreover, to explore the association of lnc‐PVT1 with disease severity, inflammation, and miR‐146a in patients with COPD. Methods A total of 80 acute exacerbation of COPD (AECOPD) patients, 80 stable COPD patients, and 80 healthy controls (HCs) were consecutively recruited. Peripheral blood samples of all participants were collected to isolate peripheral blood mononuclear cells (PBMCs), and serum: PBMCs were used to detect lnc‐PVT1 and miR‐146a by RT‐qPCR; serum was used to detect inflammatory cytokines by ELISA. Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage of COPD was assessed. Results Lnc‐PVT1 expression was highest in AECOPD patients, followed by stable COPD patients and HCs. Receiver operating characteristic curves disclosed that lnc‐PVT1 distinguished AECOPD patients and stable COPD patients from HCs, also distinguished AECOPD patients from stable COPD patients. In AECOPD patients and stable COPD patients, lnc‐PVT1 expression positively correlated with GOLD stage and levels of TNF‐α, IL‐6, IL‐8, and IL‐17. Moreover, lnc‐PVT1 was negatively correlated with miR‐146a. For miR‐146a, its expression was lowest in AECOPD patients, followed by stable COPD patients and HCs, and it predicted reduced COPD susceptibility and decreased acute exacerbation risk; meanwhile, it negatively correlated with GOLD stage and inflammatory cytokine levels in AECOPD patients and stable COPD patients. Conclusion Lnc‐PVT1 assists the disease management and acute exacerbation risk monitoring of COPD via interaction with miR‐146a.

<p>LINC00987 Ameliorates COPD by Regulating LPS-Induced Cell Apoptosis, Oxidative Stress, Inflammation and Autophagy Through Let-7b-5p/SIRT1 Axis</p>

“… 5 , 6 Accumulating studies revealed that lncRNAs participate in the pathogenesis of diseases. 7 , 8 LncRNA metastasis-associated lung adenocarcinoma transcript 1 (lncRNA MALAT1) was revealed to regulate acute respiratory distress syndrome by affecting the secretion of an inflammatory factor. 9 LncRNA plasmacytoma variant translocation (PVT1) was employed to predict COPD susceptibility based on its link with tumor necrosis factor and interleukin (IL), IL-6, IL-8, and IL-17, and microRNA-146a (miR-146a).…”

“…9 LncRNA plasmacytoma variant translocation (PVT1) was employed to predict COPD susceptibility based on its link with tumor necrosis factor and interleukin (IL), IL-6, IL-8, and IL-17, and microRNA-146a (miR-146a). 7 In addition, lnc-small nucleolar RNA host gene 1 (lnc-SNHG1) and lnc-pro-transition associated RNA (PTAR) were revealed to promote the progression of lung cancer by sponging miR-497 and miR-101, respectively. 10 , 11 In this study, LINC00987 was found to be apparently downregulated in COPD tissues.…”

Up-regulated lncRNA-PVT1 Expression in Peripheral Blood Mononuclear Cells of Patients with Coronary Artery Disease is Correlated with Decreased Interleukin-10 Production

“…MiR-146a overexpression eliminated the effects of PVT1 knockdown on prostate cancer cells (28). It should be noted that miR-146a, as a target of PVT1, has been documented as an anti-in ammatory mediator (29), which not only correlates with increased production of anti-in ammatory cytokines TGF-β1 and IL-10 (30), but also distinguishes CAD patients from NCAD patients, as mentioned above. MiR-27b-3p could be another possible mediator to justify the observed correlation between PVT1 and IL-10.…”

Comprehensive Analysis of the Profiles of Differentially Expressed mRNAs, lncRNAs, and circRNAs in Phosgene-Induced Acute Lung Injury

“…For example, Fabp4 inhibitors suppress inflammation and oxidative stress in murine and cell models of acute lung injury [ 23 ], and suppression of Fabp4 protects against rhabdomyolysis-induced acute kidney injury [ 24 ]. In chronic obstructive pulmonary disease patients, the PVT1 expression positively correlated with the GOLD stage and levels of TNF- α , IL-6, IL-8, and IL-17 [ 25 ]; PVT1 exacerbates the inflammation and cell-barrier injury during asthma by regulating miR-149 [ 26 ]. These findings suggested that Fabp4 and PVT1 might play the role in the therapeutic potential of MSCs in phosgene-induced ALI, and we will research the potential role of them in the phosgene-induced ALI in the following research.…”