Open Access

lncRNA TUG1 regulates human pulmonary microvascular endothelial cell apoptosis via sponging of the miR‑9a‑5p/BCL2L11 axis in chronic obstructive pulmonary disease

  • Authors:
    • Xichen Chen
    • Mao Mao
    • Ying Shen
    • Xueyong Jiang
    • Zhifei Yin
  • View Affiliations

  • Published online on: June 25, 2021     https://doi.org/10.3892/etm.2021.10338
  • Article Number: 906
  • Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The aim of the present study was to investigate the function of long non‑coding RNA taurine‑upregulated gene 1 (lncRNA TUG1) in chronic obstructive pulmonary disease and further assess the underlying molecular mechanisms. Flow cytometry analysis was performed to detect cell apoptosis of human pulmonary microvascular endothelial cells (HPMECs) treated with 1% cigarette smoke extract (CSE). The activity of caspase‑3 was measured using a Caspase‑3 Activity assay kit and the protein expression of cleaved caspase‑3, caspase‑3 and Bcl‑2 like 11 (BCL2L11) were measured using western blotting. Reverse transcription‑quantitative PCR (RT‑qPCR) was performed to measure the expression of TUG1 mRNA levels in the treated cells. The association between TUG1, the miR‑9a‑5p/BCL2L11 axis and with miR‑9a‑5p were predicted and verified using a dual luciferase reporter assay system. The mRNA expression of miR‑9a‑5p and BCL2L11, and the transfection efficiency were measured by RT‑qPCR. The results showed that CSE induced cell apoptosis and increased lncRNA TUG1 expression in HPMECs. CSE significantly reduced the expression of miR‑9a‑5p in HPMECs compared with the control group. TUG1‑short hairpin RNA relieved cell apoptosis induced by CSE by upregulating miR‑9a‑5p in HPMECs. The present study predicted and verified that BCL2L11 is a direct target of miR‑9a‑5p. The mRNA expression of BCL2L11 was increased in HPMECs following CSE treatment compared with the control group. miR‑9a‑5p mimic and BCL2L11‑plasmid markedly increased the expression of miR‑9a‑5p and BCL2L11, respectively. miR‑9a‑5p mimic reversed the increase in cell apoptosis induced by CSE by inhibiting BCL2L11 expression in HPMECs. To conclude, the present study demonstrated that lncRNA TUG1 exerted roles in cell apoptosis induced by CSE through modulating the miR‑9a‑5p/BCL2L11 axis.
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August-2021
Volume 22 Issue 2

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Chen X, Mao M, Shen Y, Jiang X and Yin Z: lncRNA TUG1 regulates human pulmonary microvascular endothelial cell apoptosis via sponging of the miR‑9a‑5p/BCL2L11 axis in chronic obstructive pulmonary disease. Exp Ther Med 22: 906, 2021
APA
Chen, X., Mao, M., Shen, Y., Jiang, X., & Yin, Z. (2021). lncRNA TUG1 regulates human pulmonary microvascular endothelial cell apoptosis via sponging of the miR‑9a‑5p/BCL2L11 axis in chronic obstructive pulmonary disease. Experimental and Therapeutic Medicine, 22, 906. https://doi.org/10.3892/etm.2021.10338
MLA
Chen, X., Mao, M., Shen, Y., Jiang, X., Yin, Z."lncRNA TUG1 regulates human pulmonary microvascular endothelial cell apoptosis via sponging of the miR‑9a‑5p/BCL2L11 axis in chronic obstructive pulmonary disease". Experimental and Therapeutic Medicine 22.2 (2021): 906.
Chicago
Chen, X., Mao, M., Shen, Y., Jiang, X., Yin, Z."lncRNA TUG1 regulates human pulmonary microvascular endothelial cell apoptosis via sponging of the miR‑9a‑5p/BCL2L11 axis in chronic obstructive pulmonary disease". Experimental and Therapeutic Medicine 22, no. 2 (2021): 906. https://doi.org/10.3892/etm.2021.10338