Tuberculosis and Respiratory Diseases

  • 제80권3호
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  • Pages.247-254
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  • 2017
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  • 1738-3536(pISSN)
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  • 2005-6184(eISSN)
대한결핵및호흡기학회 (The Korean Academy of Tuberculosis and Respiratory Diseases)
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ACN9 Regulates the Inflammatory Responses in Human Bronchial Epithelial Cells

  • Jeong, Jae Hoon (Department of Internal Medicine, Kangwon National University School of Medicine) ;
  • Kim, Jeeyoung (Department of Internal Medicine, Kangwon National University School of Medicine) ;
  • Kim, Jeongwoon (Department of Internal Medicine, Kangwon National University School of Medicine) ;
  • Heo, Hye-Ryeon (Department of Internal Medicine, Kangwon National University School of Medicine) ;
  • Jeong, Jin Seon (Department of Internal Medicine, Kangwon National University School of Medicine) ;
  • Ryu, Young-Joon (Department of Pathology, Kangwon National University School of Medicine) ;
  • Hong, Yoonki (Department of Internal Medicine, Kangwon National University School of Medicine) ;
  • Han, Seon-Sook (Department of Internal Medicine, Kangwon National University School of Medicine) ;
  • Hong, Seok-Ho (Department of Internal Medicine, Kangwon National University School of Medicine) ;
  • Lee, Seung-Joon (Department of Internal Medicine, Kangwon National University School of Medicine) ;
  • Kim, Woo Jin (Department of Internal Medicine, Kangwon National University School of Medicine)
  • 투고 : 2017.01.14
  • 심사 : 2017.05.04
  • 발행 : 2017.07.31
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초록

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.

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참고문헌

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