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Cho SH, Park SY, Lee EJ, et al. Regulation of CYP1A1 and Inflammatory Cytokine by NCOA7 Isoform 4 in Response to Dioxin Induced Airway Inflammation. Tuberc Respir Dis (Seoul). 2015;78(2):99-105doi: 10.4046/trd.2015.78.2.99.
Cho, S. H., Park, S. Y., Lee, E. J., Cho, Y. H., Park, H. S., Hong, S. H., & Kim, W. J. (2015). Regulation of CYP1A1 and Inflammatory Cytokine by NCOA7 Isoform 4 in Response to Dioxin Induced Airway Inflammation. Tuberculosis and respiratory diseases, 78(2), 99-105. https://doi.org/10.4046/trd.2015.78.2.99
Cho, Sung-Hwan, et al. "Regulation of CYP1A1 and Inflammatory Cytokine by NCOA7 Isoform 4 in Response to Dioxin Induced Airway Inflammation." Tuberculosis and respiratory diseases vol. 78,2 (2015): 99-105. doi: https://doi.org/10.4046/trd.2015.78.2.99
Cho SH, Park SY, Lee EJ, Cho YH, Park HS, Hong SH, Kim WJ. Regulation of CYP1A1 and Inflammatory Cytokine by NCOA7 Isoform 4 in Response to Dioxin Induced Airway Inflammation. Tuberc Respir Dis (Seoul). 2015 Apr;78(2):99-105. doi: 10.4046/trd.2015.78.2.99. Epub 2015 Apr 02. PMID: 25861343; PMCID: PMC4388907.
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Tuberc Respir Dis (Seoul). 2015 Apr;78(2):99-105. doi: 10.4046/trd.2015.78.2.99. Epub 2015 Apr 02.

Regulation of CYP1A1 and Inflammatory Cytokine by NCOA7 Isoform 4 in Response to Dioxin Induced Airway Inflammation.

Tuberculosis and respiratory diseases

Sung-Hwan Cho, Shin Young Park, Eun Jeong Lee, Yo Han Cho, Hyun Sun Park, Seok-Ho Hong, Woo Jin Kim

Affiliations

  1. Regional Center for Respiratory Diseases, Kangwon National University Hospital, Chuncheon, Korea.
  2. Department of Internal Medicine and Environmental Health Center, Kangwon National University Hospital, Kangwon National University School of Medicine, Chuncheon, Korea.
  3. Regional Center for Respiratory Diseases, Kangwon National University Hospital, Chuncheon, Korea. ; Department of Internal Medicine and Environmental Health Center, Kangwon National University Hospital, Kangwon National University School of Medicine, Chuncheon, Korea.

PMID: 25861343 PMCID: PMC4388907 DOI: 10.4046/trd.2015.78.2.99

Abstract

BACKGROUND: Aryl hydrocarbon receptor (AhR), a ligand-dependent transcription factor, binds to a wide variety of synthetic and naturally occurring compounds. AhR is involved in the regulation of inflammatory response during acute and chronic respiratory diseases. We investigated whether nuclear receptor coactivator 7 (NCOA7) could regulate transcriptional levels of AhR target genes and inflammatory cytokines in 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-treated human bronchial epithelial cells. This study was based on our previous study that NCOA7 was differentially expressed between normal and chronic obstructive pulmonary disease lung tissues.

METHODS: BEAS-2B and A549 cells grown under serum-free conditions were treated with or without TCDD (0.15 nM and 6.5 nM) for 24 hours after transfection of pCMV-NCOA7 isoform 4. Expression levels of cytochrome P4501A1 (CYP1A1), IL-6, and IL-8 were measured by quantitative real-time polymerase chain reaction.

RESULTS: The transcriptional activities of CYP1A1 and inflammatory cytokines were strongly induced by TCDD treatment in both BEAS-2B and A549 cell lines. The NCOA7 isoform 4 oppositely regulated the transcriptional activities of CYP1A1 and inflammatory cytokines between BEAS-2B and A549 cell lines.

CONCLUSION: Our results suggest that NCOA7 could act as a regulator in the TCDD-AhR signaling pathway with dual roles in normal and abnormal physiological conditions.

Keywords: Dioxins; NCOA7 Protein, Human; Pulmonary Disease, Chronic Obstructive; Receptors, Aryl Hydrocarbon

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