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.
Artículo
en Inglés
| WPRIM
| ID: wpr-78238
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.
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Factores de Transcripción
/
Transfección
/
Línea Celular
/
Citocinas
/
Interleucina-8
/
Interleucina-6
/
Receptores de Hidrocarburo de Aril
/
Citocromo P-450 CYP1A1
/
Citocromos
/
Enfermedad Pulmonar Obstructiva Crónica
Límite:
Humanos
Idioma:
Inglés
Revista:
Tuberculosis and Respiratory Diseases
Año:
2015
Tipo del documento:
Artículo
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