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Background <p>Smoking induces mitochondrial dysfunction and differential DNA methylation, which critically contribute to the progress of chronic obstructive pulmonary disease (COPD), the third leading cause worldwide. This study investigated whether abnormal mitochondrial DNA (mtDNA) methylation and gene expression are involved in mitochondrial dysfunction in airway epithelial cell lines and COPD primary epithelial cells exposed to cigarette smoke extract (CSE).</p> Methods <p>CSE exposure was performed short-term (24&#xa0;h) and long-term (up to 25 weeks). Mitochondrial function was assessed by Seahorse. MtDNA gene expressions were examined by RT-qPCR. Using mtDNA isolated from the TRIzol RNA phase, mtDNA methylation was measured by LC-MS/MS (global) and by pyrosequencing in the mitochondrial D-loop, <i>MT-CYB</i> and <i>MT-CO2</i> regions.</p> Results <p>CSE induced upregulation in mtDNA gene expression upon long-term CSE exposure of BEAS-2B cells was accompanied by mitochondrial dysfunction. No significant change in mtDNA methylation was found in these cells. Upon short-term CSE exposure, no significant changes in mtDNA gene expression, or in mtDNA methylation at individual CpN sites of the assessed regions were observed for BEAS-2B and 16HBE cells. In primary cells, the comparison between COPD and non-COPD donors (with or without CSE exposure) revealed no significant difference in mtDNA gene expression or methylation.</p> Conclusion <p>While mild changes were observed in mtDNA gene expression after CSE exposure, these responses may not act as central drivers in mitochondrial dysfunction, nor in COPD development.</p>

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The effects of cigarette smoke extract on mitochondrial function, mitochondrial gene expression and mitochondrial DNA methylation in airway epithelial cells

  • 期刊论文

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  • 发表日期：

    2025年12月24日

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  • Lin Liang,
  • Lei Wang,
  • Marnix R. Jonker,
  • Wilma Kosse,
  • Pytrick G. Jellema,
  • Marianne G. Rots,
  • Irene H. Heijink

摘要

Background

Smoking induces mitochondrial dysfunction and differential DNA methylation, which critically contribute to the progress of chronic obstructive pulmonary disease (COPD), the third leading cause worldwide. This study investigated whether abnormal mitochondrial DNA (mtDNA) methylation and gene expression are involved in mitochondrial dysfunction in airway epithelial cell lines and COPD primary epithelial cells exposed to cigarette smoke extract (CSE).

Methods

CSE exposure was performed short-term (24 h) and long-term (up to 25 weeks). Mitochondrial function was assessed by Seahorse. MtDNA gene expressions were examined by RT-qPCR. Using mtDNA isolated from the TRIzol RNA phase, mtDNA methylation was measured by LC-MS/MS (global) and by pyrosequencing in the mitochondrial D-loop, MT-CYB and MT-CO2 regions.

Results

CSE induced upregulation in mtDNA gene expression upon long-term CSE exposure of BEAS-2B cells was accompanied by mitochondrial dysfunction. No significant change in mtDNA methylation was found in these cells. Upon short-term CSE exposure, no significant changes in mtDNA gene expression, or in mtDNA methylation at individual CpN sites of the assessed regions were observed for BEAS-2B and 16HBE cells. In primary cells, the comparison between COPD and non-COPD donors (with or without CSE exposure) revealed no significant difference in mtDNA gene expression or methylation.

Conclusion

While mild changes were observed in mtDNA gene expression after CSE exposure, these responses may not act as central drivers in mitochondrial dysfunction, nor in COPD development.