Expression of microRNAs in lung homogenates in rats with chronic obstructive pulmonary disease

Abstract

To determine the expression spectrum of microRNA (miRNA) in the lung homogenate of rats with chronic obstructive pulmonary disease(COPD) or healthy rats, to look for differentially expressed miRNA, and to explore their potential role in pathogenesis of COPD. Twenty male Sprague-Dawley (SD) rats were randomly divided into normal control group and COPD model group, with 10 rats in each group. COPD rat models were reproduced by smoke inhalation as well as intratracheal instillation of lipopolysaccharide (LPS). The samples of the lung were harvested, and the histopathological examination of the right lung was carried out to evaluate the degree of lung injury. Total RNAs were isolated from the left lung. The miRNA expressions in lung tissue of rats with COPD or normal rats were determined by miRNA chip eichnology to screen the miRNA with differential expression, and hierarchical clustering analysis was made. The data were analyzed to study the expression difference of miRNAs between the two groups, and to construct the miRNA-Target network. Compared with normal control group, 20 miRNA with increased expression were found in COPD model group, the top 10 were miR-30c-2, miR-199a-5p, miR-30a, miR-145, miR-151, miR-674-5p, miR-214, miR-423, miR-28 and miR-181b, and only miR-376b-3p showed down-regulation. Hierarchical clustering analysis showed that significant differences in individual miRNA in lung tissue between rats of two groups were found. However, similar samples could not be gathered well, thus it may give rise to inconsistency during the sample preparation. Many miRNAs had multiple target genes in miRNA-Target network, such as miR-30c-2, miR-145, miR-181b, miR-181a, miR-181d, miR-199. The study reveals that there is a variance of miRNAs expression profile in lung homogenates between COPD group and the normal control group of rats, and many miRNAs have multiple target genes, such as miR-30c-2, miR-145, miR-181b, miR-181a, miR-181d, and miR-199. Therefore, the results may be valuable to centain extent for the interpretation of COPD pathogenesis.