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Sevoflurane with Low Concentration Decrease DNA Methylation on Chronic Obstructive Pulmonary Disease (COPD)-Related

Chuanxin Yang1, Libing Deng1, Fang Bao1

  • 1Department of Anesthesiology, Qingpu Branch of Zhongshan, Fudan University, Shanghai, China.

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Low-concentration sevoflurane may epigenetically benefit chronic obstructive pulmonary disease (COPD) by hypomethylating specific genes in Alveolar type II (ATII) cells. High concentrations show opposite effects, suggesting a dose-dependent epigenetic mechanism for inhaled anesthetics in COPD treatment.

Keywords:
COPDDNA methylationDNMT1REC8sevoflurane

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Area of Science:

  • Pulmonary Medicine
  • Epigenetics
  • Anesthesiology

Background:

  • Chronic obstructive pulmonary disease (COPD) is a complex respiratory illness with unclear epigenetic mechanisms influenced by inhaled anesthetics.
  • Sevoflurane's role in COPD is controversial, with varying effects depending on concentration, and its underlying epigenetic impact remains largely unknown.

Purpose of the Study:

  • To investigate the dose-dependent epigenetic effects of sevoflurane on COPD-related gene methylation in Alveolar type II (ATII) cells.
  • To elucidate the role of DNA methyltransferase 1 (DNMT1) and REC8 meiotic recombination protein (REC8) in sevoflurane-induced epigenetic modifications in COPD.

Main Methods:

  • Establishment of a lipopolysaccharide (LPS)-induced COPD rat model and isolation of ATII cells.
  • Analysis of DNA methylation patterns in the promoter regions of key COPD-related genes (Sftpa1, Napsa, Ca2, Sfta2, Lamp3, Wif1, Pgc, Etv5).
  • Assessment of DNMT1 and REC8 binding to target gene promoters and correlation with transcriptional activity.

Main Results:

  • Low-concentration (0.5%) sevoflurane induced hypomethylation of six COPD-related gene promoters in ATII cells, increasing their transcriptional activity.
  • High-concentration (2%) sevoflurane resulted in hypermethylation of the same gene promoters, decreasing transcriptional activity.
  • DNMT1 binding was crucial for these methylation changes, and REC8 specifically bound to promoters in low-concentration sevoflurane-treated cells, correlating positively with DNMT1.

Conclusions:

  • Sevoflurane exhibits a dose-dependent epigenetic effect on ATII cells in a COPD model, with low concentrations potentially offering therapeutic benefits via hypomethylation.
  • The findings highlight a novel epigenetic mechanism involving DNMT1 and REC8, providing insights into the pathogenesis and anesthetic treatment of COPD.