Regulation of CYP1A1 and Inflammatory Cytokine by NCOA7 Isoform 4 in Response to Dioxin Induced Airway Inflammation / 결핵및호흡기질환
Tuberculosis and Respiratory Diseases
; : 99-105, 2015.
Article
in English
| WPRIM (Western Pacific)
| ID: wpr-78238
Responsible library:
WPRO
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.
Full text:
Available
Database:
WPRIM (Western Pacific)
Main subject:
Transcription Factors
/
Transfection
/
Cell Line
/
Cytokines
/
Interleukin-8
/
Interleukin-6
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Receptors, Aryl Hydrocarbon
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Cytochrome P-450 CYP1A1
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Cytochromes
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Pulmonary Disease, Chronic Obstructive
Limits:
Humans
Language:
English
Journal:
Tuberculosis and Respiratory Diseases
Year:
2015
Document type:
Article