ACN9 Regulates the Inflammatory Responses in Human Bronchial Epithelial Cells.
10.4046/trd.2017.80.3.247
- Author:
Jae Hoon JEONG
1
;
Jeeyoung KIM
;
Jeongwoon KIM
;
Hye Ryeon HEO
;
Jin Seon JEONG
;
Young Joon RYU
;
Yoonki HONG
;
Seon Sook HAN
;
Seok Ho HONG
;
Seung Joon LEE
;
Woo Jin KIM
Author Information
1. Department of Internal Medicine, Kangwon National University School of Medicine, Chuncheon, Korea. pulmo2@kangwon.ac.kr
- Publication Type:Original Article
- Keywords:
Succinate Dehydrogenase;
Cadmium;
Pulmonary Disease, Chronic Obstructive;
Gene Expression;
Inflammation
- MeSH:
Cadmium;
Cytokines;
Environmental Pollutants;
Epithelial Cells*;
Gene Expression;
Gene Expression Profiling;
Humans*;
Immunohistochemistry;
In Situ Hybridization;
Inflammation;
Lung;
Lung Neoplasms;
Pulmonary Disease, Chronic Obstructive;
RNA, Messenger;
Signal Transduction;
Smoke;
Smoking;
Succinate Dehydrogenase
- From:Tuberculosis and Respiratory Diseases
2017;80(3):247-254
- CountryRepublic of Korea
- Language:English
-
Abstract:
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.
