Regulation of Cigarette Smoke (CS)-Induced Autophagy by Nrf2

Relevance to SWEHSC: 

Mucous cell metaplasia and mucus over-production are hallmarks of almost all chronic airway diseases (e.g. asthma, chronic obstructive pulmonary diseases, cystic fibrosis, etc.) and significantly increase the morbidity and mortality. No therapy is available besides the mechanical suction. We are now investigating the function and regulation of mucin genes in asthma pathogenesis using both in vivo (gene targeting model, induced mouse model of asthma, as well as tissues and secretions from asthmatic patients) and in vitro (differentiated epithelial culture and cell line) models.

Cluster of Efforts: 
  • Yin Chen, PhD
  • CSE induced LC3B-I and II as well as autophagosomes, but CSE-induced autophagy was different from that induced by starvation
  • CSE regulated LC3B-I and II at transcriptional and post-translational levels
  • Nrf2 negatively regulated LC3B and autophagy, but independent of mTOR
  • Increase of cellular GSH repressed CSE-induced LC3B and autophagosome but not mTOR
  • P62 is another Nrf2-responsive gene and responsible for repressing CSE-induced LC3B and autophagosomes
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