Hydrogen Sulfide Inhibits Bronchial Epithelial Cell Epithelial Mesenchymal Transition Through Regulating Endoplasm...

Area of Science:

• Pulmonary Medicine
• Cell Biology
• Biochemistry

Background:

• Epithelial mesenchymal transition (EMT) contributes to chronic obstructive pulmonary disease (COPD) remodeling.
• The role of hydrogen sulfide (H2S) in COPD pathogenesis and its regulation of EMT remain unclear.

Purpose of the Study:

• To investigate the effect of H2S on EMT and endoplasmic reticulum (ER) stress in COPD.
• To elucidate the underlying molecular mechanisms of H2S in regulating EMT.

Main Methods:

• Assessed ER stress and EMT markers in rat lungs, bronchial epithelial cells, and human lung tissues.
• Administered NaHS (H2S donor) and propargylglycine (inhibitor) to cigarette smoke-exposed rats.
• Utilized nicotine-exposed 16HBE cells treated with H2S donor, ER stress inhibitors, and IRE1 inhibitor.

Main Results:

• EMT and ER stress were observed in lung epithelial cells, particularly in smokers and COPD patients.
• NaHS alleviated cigarette smoke-induced lung damage, fibrosis, ER stress, and EMT in rats.
• H2S inhibited nicotine-induced ER stress, cell migration, and EMT in 16HBE cells, involving the IRE1/Smad2/3 pathway.

Conclusions:

• H2S inhibits ER stress and EMT in bronchial epithelial cells, alleviating COPD-related lung damage and fibrosis.
• The IRE1 signal pathway and Smad2/3 are implicated in the inhibitory effects of H2S on EMT.