Evaluation of the expression levels of autophagy-related genes in patients with severe and mild chronic obstructive pulmonary disease (COPD) compared with healthy controls

Abstract

Chronic obstructive pulmonary disease is the most common cause of death and disability caused by lung diseases. Chronic obstructive pulmonary disease is associated with chronic obstruction of airflow into or out of the lungs. There is increasing evidence in favor of impaired autophagy in COPD. On the one hand, its disruption can lead to the failure to clear proteins or organelles damaged by oxidative stress and accelerate the pathogenesis of COPD. On the other hand, hyperactive autophagy can lead to increased apoptotic cell death and loss of cilia, and finally emphysema in COPD patients. Methods and Materials: From 40 patients with mild COPD, 40 patients with severe COPD, and 40 healthy controls, 5 cc of blood containing anticoagulant was taken to isolate PBMC. To check the expression level of autophagy genes, Real Time-PCR technique with specific primers was used. Western blot technique was also used to measure the expression of autophagy proteins. Finally, the statistical analysis of the results was done with appropriate statistical tests and b using SPSS statistical software. Results: The expression of FOXO1, FOXO6, Beclin, LC3, Atg5, Atg6, Atg7, and Atg8 genes is significantly higher in the mild and severe COPD group than in the healthy control group, and this increase was much higher in the severe COPD group. which indicates an increase in autophagy in these patients. As can be seen, the expression of all these genes is significantly higher in the mild and severe COPD group than in the healthy control group, and this increase was much higher in the severe COPD group, which indicates an increase in autophagy in these patients. The level of Beclin and LC3 protein expression in peripheral blood mononuclear cell samples of severe COPD patients is significantly higher than the mild COPD group, which indicates the important role of these proteins in the pathogenesis and severity of COPD disease.