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

Cho SH, Park SY, Lee EJ, Cho YH, Park HS, Hong SH, Kim WJ - Tuberc Respir Dis (Seoul) (2015)

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Regional Center for Respiratory Diseases, Kangwon National University Hospital, Chuncheon, Korea.

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.

No MeSH data available.


Related in: MedlinePlus

Human nuclear receptor coactivator 7 isoform expression based on RNA-sequencing. Isoforms expression in normal control (NC) and chronic obstructive pulmonary disease (COPD) human lung tissues. FPKM fold change was the ratio of average FPKM between COPD and NC.
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Figure 1: Human nuclear receptor coactivator 7 isoform expression based on RNA-sequencing. Isoforms expression in normal control (NC) and chronic obstructive pulmonary disease (COPD) human lung tissues. FPKM fold change was the ratio of average FPKM between COPD and NC.

Mentions: From the RNA-sequencing database, the RNA-sequencing results showed higher transcript levels of NCOA7 isoform 4 in COPD lung tissues compared to the normal control tissues (Figure 1).


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

Cho SH, Park SY, Lee EJ, Cho YH, Park HS, Hong SH, Kim WJ - Tuberc Respir Dis (Seoul) (2015)

Human nuclear receptor coactivator 7 isoform expression based on RNA-sequencing. Isoforms expression in normal control (NC) and chronic obstructive pulmonary disease (COPD) human lung tissues. FPKM fold change was the ratio of average FPKM between COPD and NC.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4388907&req=5

Figure 1: Human nuclear receptor coactivator 7 isoform expression based on RNA-sequencing. Isoforms expression in normal control (NC) and chronic obstructive pulmonary disease (COPD) human lung tissues. FPKM fold change was the ratio of average FPKM between COPD and NC.
Mentions: From the RNA-sequencing database, the RNA-sequencing results showed higher transcript levels of NCOA7 isoform 4 in COPD lung tissues compared to the normal control tissues (Figure 1).

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Regional Center for Respiratory Diseases, Kangwon National University Hospital, Chuncheon, Korea.

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.

No MeSH data available.


Related in: MedlinePlus