ACN9 Regulates the Inflammatory Responses in Human Bronchial Epithelial Cells

Tuberculosis and Respiratory Diseases

article

Jae Hoon Jeong¹  Jeeyoung Kim¹  Jeongwoon Kim¹  Hye-Ryeon Heo¹  Jin Seon Jeong¹  Young-Joon Ryu²  Yoonki Hong¹  Seon-Sook Han¹  Seok-Ho Hong¹  Seung-Joon Lee¹  Woo Jin Kim¹ 

[1] Department of Internal Medicine, Kangwon National University School of Medicine;Department of Pathology, Kangwon National University School of Medicine

关键词: Succinate Dehydrogenase;    Cadmium;    Pulmonary Disease;    Chronic Obstructive;    Gene Expression;    Inflammation;   

DOI  :  10.4046/trd.2017.80.3.247

学科分类：医学（综合）

来源: The Korean Academy of Tuberculosis and Respiratory Diseases

【 摘 要 】

Background Airway epithelial cells are the first line of defense, against pathogens and environmental pollutants, in the lungs. Cellular stress by cadmium (Cd), resulting in airway inflammation, is assumed to be directly involved in tissue injury, linked to the development of lung cancer, and chronic obstructive pulmonary disease (COPD). We had earlier shown that ACN9 (chromosome 7q21), is a potential candidate gene for COPD, and identified significant interaction with smoking, based on genetic studies. However, the role of ACN9 in the inflammatory response, in the airway cells, has not yet been reported. Methods We first checked the anatomical distribution of ACN9 in lung tissues, using mRNA in situ hybridization, and immunohistochemistry. Gene expression profiling in bronchial epithelial cells (BEAS-2B), was performed, after silencing ACN9 . We further tested the roles of ACN9, in the intracellular mechanism, leading to Cd-induced production, of proinflammatory cytokines in BEAS-2B. Results ACN9 was localized in lymphoid, and epithelial cells, of human lung tissues. ACN9 silencing, led to differential expression of 216 genes. Pathways of sensory perception to chemical stimuli, and cell surface receptor-linked signal transduction, were significantly enriched. ACN9 silencing, further increased the expression of proinflammatory cytokines, in BEAS-2B after Cd exposure. Conclusion Our findings suggest, that ACN9 may have a role, in the inflammatory response in the airway.

【 授权许可】

CC BY-NC