Identification of specific gene modules in mouse lung tissue exposed to cigarette smoke.

Yong-Hua Xing,Jian-Guo Li,Jun-Ling Zhang,Lu Lu,Yue-Ying Wang,Cheng-Cheng Li,Guo-Shun Xu,Zhu-Bo Zhang,De-Guan Li,Ai-Min Meng,Song Huang

doi:10.7314/apjcp.2015.16.10.4251

Abstract

Exposure to cigarette may affect human health and increase risk of a wide range of diseases including pulmonary diseases, such as chronic obstructive pulmonary disease (COPD), asthma, lung fibrosis and lung cancer. However, the molecular mechanisms of pathogenesis induced by cigarettes still remain obscure even with extensive studies. With systemic view, we attempted to identify the specific gene modules that might relate to injury caused by cigarette smoke and identify hub genes for potential therapeutic targets or biomarkers from specific gene modules. The dataset GSE18344 was downloaded from the Gene Expression Omnibus (GEO) and divided into mouse cigarette smoke exposure and control groups. Subsequently, weighted gene co-expression network analysis (WGCNA) was used to construct a gene co-expression network for each group and detected specific gene modules of cigarette smoke exposure by comparison. A total of ten specific gene modules were identified only in the cigarette smoke exposure group but not in the control group. Seven hub genes were identified as well, including Fip1l1, Anp32a, Acsl4, Evl, Sdc1, Arap3 and Cd52. Specific gene modules may provide better understanding of molecular mechanisms, and hub genes are potential candidates of therapeutic targets that may possible improve development of novel treatment approaches.

Highlights

Cigarette smoke has multiple, highly diverse effects on human health, and leads more than 5 million deaths each year (Pirini et al, 2015)
Total 8146 genes were identified as DEs by comparing the cigarette smoke exposure group with control group
Total 28 gene modules were identified in the control network and 38 gene modules were detected in cigarette smoke exposure network (Figure 1)

Summary

Introduction

Highly diverse effects on human health, and leads more than 5 million deaths each year (Pirini et al, 2015). Cigarette smoking induces the serve progressive noncancerous lung disease, such as pulmonary fibrosis and emphysema by elevating ROS levels and impairing the DNA stability (Morse and Rosas, 2014). Most of these studies rely on the epidemical studies and animal models or individual cell types in vitro that based on reductionist approach that resort to one pathogenic factor for one disease. Exposure to cigarette may affect human health and increase risk of a wide range of diseases including pulmonary diseases, such as chronic obstructive pulmonary disease (COPD), asthma, lung fibrosis and lung cancer. Conclusions: Specific gene modules may provide better understanding of molecular mechanisms, and hub genes are potential candidates of therapeutic targets that may possible improve development of novel treatment approaches

Methods

Results

Conclusion