Effect of hypoxia and cigarette smoke on hypoxia-inducible factor 1α (HIF-1α) and heat shock protein 72 (HSP72) system of alveolar epithelial cells

Smoking is the main risk factor of alvolar destruction in emphyseama/COPD. In COPD airway obstruction causes hypoventilated areas in the lung leading to alveolar hypoxia. HIF-1 α plays a key role in the defense against hypoxic cellular damage. The inducible HSP72 has a central role in the maintenance of cell integrity, apoptosis and cellular immunity. It is unknown, what role HIF-1α and HSP72 play in cell damage caused by hypoxia and cigarette smoke. HIF1α and HSP72 mRNA expression using RT-PCR of immortalized alveolar epithelial cells (A549) was analyzed using hypoxia (FiO2 20,9% (control); 13±1%; 6±1%; 1±1%) and treatment with cigarette smoke extract (CSE). Under hypoxic conditions cell count grew significantly (FiO2 13±1%: 13,33x105; FiO2 6±1%:13,2x105; FiO2 1±1%: 12,86x105 vs. normoxia FiO2 20,9%: 7,73x105; p Hypoxia increases, whereas CSE treatment decreases alveolar epithelial cell count. HSP72 mRNA decreases following hypoxic or CSE induced cellular stress, while severe hypoxia and CSE treatment decreases HIF-1α mRNA expression of A549 cells.