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The ER stress-mediated decrease in DDAH1 expression is involved in formaldehyde-induced apoptosis in lung epithelial

Seul Ki Lim1, Hyeon Choi, Min Jung Park

  • 1Bio-therapy Human Resources Center, College of Veterinary Medicine, Chonnam National University, Gwangju 500-757, South Korea.

Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association
|October 22, 2013
PubMed
Summary
This summary is machine-generated.

Formaldehyde (FA) induces lung epithelial cell death by decreasing dimethylarginine dimethylaminohydrolase 1 (DDAH1) expression, leading to endoplasmic reticulum (ER) stress. DDAH1 overexpression prevents this FA-induced apoptosis.

Keywords:
ApoptosisDDAH1DDAH2ER-stressFormaldehydeLung epithelial cells

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Area of Science:

  • Toxicology
  • Cell Biology
  • Molecular Biology

Background:

  • Formaldehyde (FA) is a respiratory toxicant.
  • Nitric oxide (NO) dysfunction is linked to respiratory diseases.
  • The role of dimethylarginine dimethylaminohydrolase (DDAH) in FA-induced lung cell death was unknown.

Purpose of the Study:

  • To investigate FA's effect on DDAH expression and ER stress in lung epithelial cells.
  • To determine if DDAH overexpression prevents FA-induced ER stress and apoptosis.

Main Methods:

  • A549 lung epithelial cells were treated with FA.
  • DDAH expression, ER stress markers, and apoptosis-related proteins were analyzed.
  • DDAH1 and DDAH2 overexpression were used to assess protective effects.

Main Results:

  • FA decreased cell viability and DDAH1/DDAH2 expression.
  • FA induced ER stress (IRE1α, PERK, eIF-2α phosphorylation) and apoptosis (increased Bax, CHOP, cleaved PARP/caspase-3; decreased Bcl-2).
  • DDAH1 overexpression, but not DDAH2, protected against FA-induced cell death and ER stress.

Conclusions:

  • FA induces lung epithelial cell apoptosis by reducing DDAH1 expression.
  • This reduction triggers endoplasmic reticulum stress.
  • DDAH1 plays a critical protective role against formaldehyde-induced lung cell injury.