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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

Effect of overexpression of nuclear receptor coactivator 7 (NCOA7) isoform 4 on cytochrome P4501A1 (CYP1A1) mRNA expression. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)-induced expression of CYP1A1 mRNA in BEAS-2B (A) and A549 (B) cell cultures. Cells were transfected with mock control vector or the NCOA7 isoform 4 for 24 hours prior to the addition of TCDD (0.15 nM and 0.65 nM) for 24 hours. Bars represent mean±SD. *p<0.05 indicating statistical significance between the mock control- and NCOA7 isoform 4- transfected cells.
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Figure 2: Effect of overexpression of nuclear receptor coactivator 7 (NCOA7) isoform 4 on cytochrome P4501A1 (CYP1A1) mRNA expression. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)-induced expression of CYP1A1 mRNA in BEAS-2B (A) and A549 (B) cell cultures. Cells were transfected with mock control vector or the NCOA7 isoform 4 for 24 hours prior to the addition of TCDD (0.15 nM and 0.65 nM) for 24 hours. Bars represent mean±SD. *p<0.05 indicating statistical significance between the mock control- and NCOA7 isoform 4- transfected cells.

Mentions: We examined the effect of NCOA7 isoform 4 on the transcriptional activity of CYP1A1 in BEAS-2B cells and A549 cells. BEAS-2B and A549 cells were transfected with NCOA7-GFP and GFP (as control) expression plasmids. NCOA7-GFP level was determined by Western blot analysis (Appendix 1). After transfection, the amount of CYP1A1 transcript was increased by treatment of either 0.15 or 0.65 nM TCDD in both cell lines. Expression level of CYP1A1 mRNA was significantly lower in NCOA7-transfected cells compared to the mock-transfected cells in BEAS-2B cell cultures treated with 0.65 nM TCDD (p<0.05) (Figure 2A). However, expression level of CYP1A1 mRNA was significantly higher in NCOA7-transfected cells compared to the mock-transfected cells in A549 cell cultures treated with 0.65 nM TCDD (p<0.05) (Figure 2B).


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)

Effect of overexpression of nuclear receptor coactivator 7 (NCOA7) isoform 4 on cytochrome P4501A1 (CYP1A1) mRNA expression. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)-induced expression of CYP1A1 mRNA in BEAS-2B (A) and A549 (B) cell cultures. Cells were transfected with mock control vector or the NCOA7 isoform 4 for 24 hours prior to the addition of TCDD (0.15 nM and 0.65 nM) for 24 hours. Bars represent mean±SD. *p<0.05 indicating statistical significance between the mock control- and NCOA7 isoform 4- transfected cells.
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4388907&req=5

Figure 2: Effect of overexpression of nuclear receptor coactivator 7 (NCOA7) isoform 4 on cytochrome P4501A1 (CYP1A1) mRNA expression. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)-induced expression of CYP1A1 mRNA in BEAS-2B (A) and A549 (B) cell cultures. Cells were transfected with mock control vector or the NCOA7 isoform 4 for 24 hours prior to the addition of TCDD (0.15 nM and 0.65 nM) for 24 hours. Bars represent mean±SD. *p<0.05 indicating statistical significance between the mock control- and NCOA7 isoform 4- transfected cells.
Mentions: We examined the effect of NCOA7 isoform 4 on the transcriptional activity of CYP1A1 in BEAS-2B cells and A549 cells. BEAS-2B and A549 cells were transfected with NCOA7-GFP and GFP (as control) expression plasmids. NCOA7-GFP level was determined by Western blot analysis (Appendix 1). After transfection, the amount of CYP1A1 transcript was increased by treatment of either 0.15 or 0.65 nM TCDD in both cell lines. Expression level of CYP1A1 mRNA was significantly lower in NCOA7-transfected cells compared to the mock-transfected cells in BEAS-2B cell cultures treated with 0.65 nM TCDD (p<0.05) (Figure 2A). However, expression level of CYP1A1 mRNA was significantly higher in NCOA7-transfected cells compared to the mock-transfected cells in A549 cell cultures treated with 0.65 nM TCDD (p<0.05) (Figure 2B).

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