Expression of long non-coding RNAs and protein-coding genes involved in cellular senescence in patients with chronic obstructive pulmonary disease

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Chronic obstructive pulmonary disease (COPD) is a complex chronic heterogeneous respiratory inflammatory disease. The disease develops as a result of complex interaction of molecular genetic factors, a network of epigenetic regulators and environmental exposure. COPD pathogenesis may also involve dysregulation of stress responses preventing cellular senescence, encompassing a wide range of signaling pathways and their epigenetic regulators, including long noncoding RNAs (lncRNAs). In order to assess the contribution of genes involved in key signaling pathways related to cellular senescence to the molecular pathogenesis of COPD the expression profile of long non-coding RNA (TP53TG1, LINC00342, H19, MALAT1, DNM3OS, MEG3) and protein-coding genes (PTEN, TGFB2, FOXO3, KEAP1) in peripheral blood mononuclear cells of COPD patients (n = 92) and controls (n = 81) was evaluated. Significant downregulation of lncRNAs TP53TG1, DNM3OS and mRNA TGFB2 expression levels was found. The expression levels of ncRNAs MALAT1 and LINC00342 were upregulated in COPD patients. Based on the results of multiple regression and ROC-analysis, a highly informative prognostic model was determined, which included simultaneous expression level assessment of TP53TG1 and TGFB2 (AUC = 0.92). A positive correlation of MALAT1, DNM3OS, TGFB2, FOXO3 and KEAP1 expression levels with lung function parameters which reflect the disease progression was established. The differentially expressed lncRNAs (TP53TG1, LINC00342, DNM3OS, MALAT1) and protein-coding gene TGFB2 detected in the study functionally act as regulators of apoptosis, inflammation, fibrogenesis and epithelial-mesenchymal transition, indicating an active role of cellular senescence processes in the molecular pathogenesis of COPD.

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作者简介

V. Markelov

Ufa Federal Research Centre of the Russian Academy of Sciences (IBG UFRC RAS); Bashkir State Medical University

Email: guly_kory@mail.ru

Institute of Biochemistry and Genetics

俄罗斯联邦, Ufa, 450054; Ufa, 450008

G. Korytina

Ufa Federal Research Centre of the Russian Academy of Sciences (IBG UFRC RAS); Bashkir State Medical University

编辑信件的主要联系方式.
Email: guly_kory@mail.ru

Institute of Biochemistry and Genetics

俄罗斯联邦, Ufa, 450054; Ufa, 450008

Y. Aznabaeva

Bashkir State Medical University

Email: guly_kory@mail.ru
俄罗斯联邦, Ufa, 450008

I. Gibadullin

Bashkir State Medical University

Email: guly_kory@mail.ru
俄罗斯联邦, Ufa, 450008

L. Akhmadishina

Ufa Federal Research Centre of the Russian Academy of Sciences (IBG UFRC RAS); Ufa State Petroleum Technological University

Email: guly_kory@mail.ru

Institute of Biochemistry and Genetics

俄罗斯联邦, Ufa, 450054; Ufa, 450064

T. Nasibullin

Ufa Federal Research Centre of the Russian Academy of Sciences (IBG UFRC RAS)

Email: guly_kory@mail.ru

Institute of Biochemistry and Genetics

俄罗斯联邦, Ufa, 450054

O. Kochetova

Ufa Federal Research Centre of the Russian Academy of Sciences (IBG UFRC RAS)

Email: guly_kory@mail.ru

Institute of Biochemistry and Genetics

俄罗斯联邦, Ufa, 450054

A. Avzaletdinov

Bashkir State Medical University

Email: guly_kory@mail.ru
俄罗斯联邦, Ufa, 450008

N. Zagidullin

Bashkir State Medical University

Email: guly_kory@mail.ru
俄罗斯联邦, Ufa, 450008

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2. Fig. S1
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4. Appendix
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5. Fig. 1. Relative expression (presented as lg Fold Change (2-ΔΔCt)) of lncRNA and mRNA in COPD patients and control individuals. Results are presented as median and 25–75% interquartile range (median (25–75% IQR), P – in the Mann–Whitney U test.

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6. Fig. 2. ROC analysis of the prognostic significance of lncRNA and mRNA, the relative expression level of which is altered in MNCs of COPD patients. AUC: area under the curve. a – DNM3OS lncRNA; б – LINC000342 lncRNA; в – MALAT1 lncRNA; г – TP53TG1 lncRNA; д – TGFB2 mRNA; е – prognostic model that includes simultaneous assessment of the expression level of TP53TG1 and TGFB2 lncRNA.

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