Knockdown of GNL3L Alleviates the Progression of COPD Through Inhibiting the ATM/p53 Pathway.

ABSTRACT:

Background

Chronic obstructive pulmonary disease (COPD) is a persistent chronic bronchitis disease, and its potential biomarkers have not been fully expounded. This study aims to explore the role of Guanine nucleotide binding protein like-3-like (GNL3L) in COPD induced by cigarette smoking (CS) in vivo.

Methods

Two microarray datasets of COPD were selected to screen differentially expressed genes (DEGs). A protein-protein interaction network was constructed to find hub genes. The COPD model was conducted using CS/LPS-induced mouse and cigarette smoke extract induced human bronchial epithelial cells. The pathological changes of lung tissue in mice were observed by hematoxylin-eosin staining and mean linear intercept. Cell viability was measured by CCK8 assay. Oxidative stress

SUBMITTER: Cai Q 

PROVIDER: S-EPMC10664632 | biostudies-literature | 2023

REPOSITORIES: biostudies-literature