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Analysis of expression profile of long non-coding RNA in patients with idiopathic and COVID-19-induced pulmonary fibrosis

https://doi.org/10.24060/2076-3093-2023-13-4-1

Abstract

Introduction. Idiopathic pulmonary fibrosis (IPF) comprises an interstitial lung disease with unclear pathogenesis, rapid progression, and no effective treatment. Pulmonary fibrosis is reported to be one of the most severe complications induced by a new coronavirus infection COVID-19. The mechanisms triggering pulmonary fibrosis and leading to its rapid progression remain substantially unclear. Evidence suggests that immune and genetic factors contribute to the development of this disease. Among the latter, the role of long non-coding RNAs (dnRNAs) has been actively studied to date. Materials and methods. Considering the role of TP53TG1, LINC00342, H19, MALAT1, DNM3OS, and MEG3 dnRNAs as regulators of signaling pathways associated with fibroblast activation and epithelial-mesenchymal transition, the authors analyzed the expression level of selected dnRNAs in lung tissue and blood mononuclear cells of patients with IPF (N = 12), post-COVID-19 pulmonary fibrosis (N = 14), and in control group (N = 27). Results and discussion. Blood mononuclear cells in patients with IPF and post-COVID-19 PF revealed similar patterns of TP53TG1 and MALAT1 dnRNA expression. The level of relative expression of MALAT1 was significantly higher in patients with IPF (Fold Change=3.207, P = 0.0005) and with post-COVID-19 PF (Fold Change=9.854, P = 0.0003), while the relative expression level of TP53TG1 reduced in patients with IPF (Fold Change=0.4308, P = 0.0313) and with post-COVID-19 PF (Fold Change=0.1888, P = 0.0003 in blood mononuclear cells, Fold Change=0.1791, P = 0.0237 in lung tissue). Increased expression of DNM3OS in blood mononuclear cells (Fold Change=12.899, P = 0.0016) and lung tissue (Fold Change=9.527, P = 0.0001), LINC00342 (Fold Change=2.221, P = 0.0309) in blood mononuclear cells was revealed only in patients with IPF. Conclusion. Evaluation of the dnRNA expression profile of TP53TG1, LINC00342, MALAT1 and DNM3OS in blood mononuclei can be used as an informative and non-invasive biomarker in IPF and post COVID-19 PF.

About the Authors

G. F. Korytina
Bashkir State Medical University; Institute of Biochemistry and Genetics, Ufa Federal Research Centre of the Russian Academy of Sciences
Russian Federation

Gulnaz F. Korytina — Dr. Sci. (Biol.), Assoc. Prof., Department of Biology, Chief Researcher, Physiological Genetics Laboratory

Ufa



I. A. Gibadullin
Bashkir State Medical University
Russian Federation

Irshat A. Gibadullin — Postgraduate Student, Department of Hospital Surgery

Ufa



Sh. R. Zulkarneev
Bashkir State Medical University
Russian Federation

Shamil R. Zulkarneev — 5th year Student, Medical Faculty

Ufa



A. I. Gimazovа
State Novosibirsk Regional Clinical Hospital
Russian Federation

Aliya I. Gimazova — Thoracic Surgery Unit

Novosibirsk



V. A. Markelov
Bashkir State Medical University; Institute of Biochemistry and Genetics, Ufa Federal Research Centre of the Russian Academy of Sciences
Russian Federation

Vitaliy A. Markelov — Postgraduate Student, Physiological Genetics Laboratory, Medical Research Assistant, Cell Culture Laboratory

Ufa



R. Kh. Zulkarneev
Bashkir State Medical University
Russian Federation

Rustem Kh. Zulkarneev — Dr. Sci. (Med.), Prof., Department of Propaedeutics of Internal Diseases

Ufa



A. A. Bakirov
Bashkir State Medical University
Russian Federation

Anvar A. Bakirov — Dr. Sci. (Med.), Prof., Department of General Surgery with Transplantology and X-ray Diagnostics Courses for Advanced Professional Education

Ufa



A. M. Avzaletdinov
Bashkir State Medical University; Clinic of Bashkir State Medical University
Russian Federation

Artur M. Avzaletdinov — Dr. Sci. (Med.), Department of Hospital Surgery, Thoracic Surgery Unit

Ufa



N. Sh. Zagidullin
Bashkir State Medical University
Russian Federation

Naufal Sh. Zagidullin — Dr. Sci. (Med.), Prof., Department of Propaedeutics of Internal Diseases

Ufa



References

1. Avdeev S.N., Aisanov Z.R., Belevskiy A.S., Ilkovich M.M., Kogan E.A., Merzhoeva Z.M., et al. Federal clinical guidelines on diagnosis and treatment of idiopathic pulmonary fibrosis. Pul’monologiya. 2022;32(3):473–95 (In Russ.). DOI: 10.18093/0869-0189-2022-32-3-473-495

2. Giacomelli C., Piccarducci R., Marchetti L., Romei C., Martini C. Pulmonary fibrosis from molecular mechanisms to therapeutic interventions: lessons from post-COVID-19 patients. Biochem Pharmacol. 2021;193:114812. DOI: 10.1016/j.bcp.2021.114812

3. Richeldi L., Collard H.R., Jones M.G. Idiopathic pulmonary fibrosis. Lancet. 2017;389(10082):1941–52. DOI: 10.1016/S0140-6736(17)30866-8

4. Tanni S.E., Fabro A.T., de Albuquerque A., Ferreira E.V.M., Verrastro C.G.Y., Sawamura M.V.Y., et al. Pulmonary fibrosis secondary to COVID-19: a narrative review. Expert Rev Respir Med. 2021;15(6):791–803. DOI: 10.1080/17476348.2021.1916472

5. Phan T.H.G., Paliogiannis P., Nasrallah G.K., Giordo R., Eid A.H., Fois A.G., et al. Emerging cellular and molecular determinants of idiopathic pulmonary fibrosis. Cell Mol Life Sci. 2021;78(5):2031–57. DOI: 10.1007/s00018-020-03693-7

6. Michalski J.E., Schwartz D.A. Genetic risk factors for idiopathic pulmonary fibrosis: insights into immunopathogenesis. J Inflamm Res. 2021;13:1305–18. DOI: 10.2147/JIR.S280958

7. Tirelli C., Pesenti C., Miozzo M., Mondoni M., Fontana L., Centanni S. The genetic and epigenetic footprint in idiopathic pulmonary fibrosis and familial pulmonary fibrosis: a state-of-the-art review. Diagnostics (Basel). 2022;12(12):3107. DOI: 10.3390/diagnostics12123107

8. Zhang S., Chen H., Yue D., Blackwell T.S., Lv C., Song X. Long noncoding RNAs: Promising new targets in pulmonary fibrosis. J Gene Med. 2021;23(3):e3318. DOI: 10.1002/jgm.3318

9. Zhang P., Wu W., Chen Q., Chen M. Non-Coding RNAs and their Integrated Networks. J Integr Bioinform. 2019;16(3):20190027. DOI: 10.1515/jib-2019-0027

10. Yan W., Wu Q., Yao W., Li Y., Liu Y., Yuan J., et al. MiR-503 modulates epithelial-mesenchymal transition in silica-induced pulmonary fibrosis by targeting PI3K p85 and is sponged by lncRNA MALAT1. Sci Rep. 2017;7(1):11313. DOI: 10.1038/s41598-017-11904-8

11. Raghu G., Remy-Jardin M., Richeldi L., Thomson C.C., Inoue Y., Johkoh T., et al. Idiopathic pulmonary fibrosis (an update) and progressive pulmonary fibrosis in adults: an official ATS/ERS/JRS/ALAT Clinical Practice Guideline. Am J Respir Crit Care Med. 2022;205(9):e18–47. DOI: 10.1164/rccm.202202-0399ST.

12. Duong-Quy S., Vo-Pham-Minh T., Tran-Xuan Q., Huynh-Anh T., Vo-Van T., Vu-Tran-Thien Q., et al. Post-COVID-19 pulmonary fibrosis: facts-challenges and futures: a narrative review. Pulm Ther. 2023;9(3):295–307. DOI: 10.1007/s41030-023-00226-y

13. Livak K.J., Schmittgen T.D. Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method. Methods. 2001;25(4):402–8. DOI: 10.1006/meth.2001.1262

14. Ghafouri-Fard S., Abak A., Talebi S.F., Shoorei H., Branicki W., Taheri M., et al. Role of miRNA and lncRNAs in organ fibrosis and aging. Biomed Pharmacother. 2021;143:112132. DOI: 10.1016/j.biopha.2021.112132

15. Lai X., Zhong J., Zhang A., Zhang B., Zhu T., Liao R. Focus on long non-coding RNA MALAT1: Insights into acute and chronic lung diseases. Front Genet. 2022;13:1003964. DOI: 10.3389/fgene.2022.1003964

16. Wang F., Li P., Li F.S. Integrated analysis of a gene correlation network identifies critical regulation of fibrosis by lncRNAs and TFs in idiopathic pulmonary fibrosis. Biomed Res Int. 2020;2020:6537462. DOI: 10.1155/2020/6537462

17. Xiao H., Liu Y., Liang P., Wang B., Tan H., Zhang Y., et al. TP53TG1 enhances cisplatin sensitivity of non-small cell lung cancer cells through regulating miR-18a/PTEN axis. Cell Biosci. 2018;8:23. DOI: 10.1186/s13578-018-0221-7

18. Sun J., Guo Y., Chen T., Jin T., Ma L., Ai L., et al. Systematic analyses identify the anti-fibrotic role of lncRNA TP53TG1 in IPF. Cell Death Dis. 2022;13(6):525. DOI: 10.1038/s41419-022-04975-7

19. Savary G., Dewaeles E., Diazzi S., Buscot M., Nottet N., Fassy J., et al. The long noncoding RNA DNM3OS is a reservoir of fibromirs with major functions in lung fibroblast response to TGF-β and pulmonary fibrosis. Am J Respir Crit Care Med. 2019;200(2):184–98. DOI: 10.1164/rccm.201807-1237OC

20. Fan Q., Jian Y. MiR-203a-3p regulates TGF-β1-induced epithelial-mesenchymal transition (EMT) in asthma by regulating Smad3 pathway through SIX1. Biosci Rep. 2020;40(2):BSR20192645. DOI: 10.1042/BSR20192645


Review

For citations:


Korytina G.F., Gibadullin I.A., Zulkarneev Sh.R., Gimazovа A.I., Markelov V.A., Zulkarneev R.Kh., Bakirov A.A., Avzaletdinov A.M., Zagidullin N.Sh. Analysis of expression profile of long non-coding RNA in patients with idiopathic and COVID-19-induced pulmonary fibrosis. Creative surgery and oncology. 2023;13(4):284-291. (In Russ.) https://doi.org/10.24060/2076-3093-2023-13-4-1

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ISSN 2076-3093 (Print)
ISSN 2307-0501 (Online)