Vasopressin inhibits mitogen-activated protein kinases and activated protein-1 in macrophages

Yu Long Chen, Ya Ying Chang, Ming Chang Kao, Chun Jen Huang

研究成果: 雜誌貢獻文章

1 引文 (Scopus)

摘要

Objectives We have previously shown that vasopressin could inhibit the upregulation of inflammatory mediators. Expression of inflammatory mediators is tightly regulated by the upstream transcriptional pathway mitogen-activated protein kinases (MAPKs) and activated protein-1 (AP-1). In this study, we elucidated whether vasopressin could inhibit the upregulation of MAPKs/AP-1. Methods Murine macrophages (RAW264.7 cells) randomly received lipopolysaccharide (LPS; 100 ng/mL) or LPS plus vasopressin (1000 pg/mL) (designated as the LPS and the LPS+V groups, respectively). Control groups were run simultaneously. For MAPKs, cells were harvested at 0 minutes, 15 minutes, 30 minutes, 45 minutes, and 60 minutes after reaction. For AP-1, cells were harvested at 60 minutes after reaction. Between-group differences in MAPKs (i.e., extracellular regulated kinase, c-Jun N-terminal kinase, and p38 MAPK) and AP-1 expressions were compared. Results Immunoblotting assay data revealed that extracellular regulated kinase concentrations of the LPS +V group that harvested at 45 minutes and 60 minutes, but not at 15 minutes and 30 minutes, were significantly lower than those of the LPS group (p = 0.005 and p = 0.013). C-Jun N-terminal kinase concentrations of the LPS+V group that harvested at 15 minutes, 30 minutes, 45 minutes, and 60 minutes were also significantly lower than those of the LPS group (all p < 0.001). Concentrations of p38 MAPK of the LPS+V group that harvested at 15 minutes, 30 minutes, and 45 minutes, but not at 60 minutes, were also significantly lower than those of the LPS group (all p < 0.001). In addition, immunohistochemistry assay revealed that the AP-1 fluorescence signals of the LPS+V group were weaker than those of the LPS group. Conclusion Vasopressin inhibits MAPKs and AP-1 in endotoxin-activated macrophages.
原文英語
文章編號223
頁(從 - 到)81-84
頁數4
期刊Acta Anaesthesiologica Taiwanica
53
發行號3
DOIs
出版狀態已發佈 - 九月 1 2015
對外發佈Yes

指紋

Mitogen-Activated Protein Kinases
Vasopressins
Macrophages
Proteins
Phosphotransferases
p38 Mitogen-Activated Protein Kinases
Up-Regulation
JNK Mitogen-Activated Protein Kinases
Immunoblotting
Endotoxins
Lipopolysaccharides
Fluorescence
Immunohistochemistry
Control Groups

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

引用此文

Vasopressin inhibits mitogen-activated protein kinases and activated protein-1 in macrophages. / Chen, Yu Long; Chang, Ya Ying; Kao, Ming Chang; Huang, Chun Jen.

於: Acta Anaesthesiologica Taiwanica, 卷 53, 編號 3, 223, 01.09.2015, p. 81-84.

研究成果: 雜誌貢獻文章

Chen, Yu Long ; Chang, Ya Ying ; Kao, Ming Chang ; Huang, Chun Jen. / Vasopressin inhibits mitogen-activated protein kinases and activated protein-1 in macrophages. 於: Acta Anaesthesiologica Taiwanica. 2015 ; 卷 53, 編號 3. 頁 81-84.
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abstract = "Objectives We have previously shown that vasopressin could inhibit the upregulation of inflammatory mediators. Expression of inflammatory mediators is tightly regulated by the upstream transcriptional pathway mitogen-activated protein kinases (MAPKs) and activated protein-1 (AP-1). In this study, we elucidated whether vasopressin could inhibit the upregulation of MAPKs/AP-1. Methods Murine macrophages (RAW264.7 cells) randomly received lipopolysaccharide (LPS; 100 ng/mL) or LPS plus vasopressin (1000 pg/mL) (designated as the LPS and the LPS+V groups, respectively). Control groups were run simultaneously. For MAPKs, cells were harvested at 0 minutes, 15 minutes, 30 minutes, 45 minutes, and 60 minutes after reaction. For AP-1, cells were harvested at 60 minutes after reaction. Between-group differences in MAPKs (i.e., extracellular regulated kinase, c-Jun N-terminal kinase, and p38 MAPK) and AP-1 expressions were compared. Results Immunoblotting assay data revealed that extracellular regulated kinase concentrations of the LPS +V group that harvested at 45 minutes and 60 minutes, but not at 15 minutes and 30 minutes, were significantly lower than those of the LPS group (p = 0.005 and p = 0.013). C-Jun N-terminal kinase concentrations of the LPS+V group that harvested at 15 minutes, 30 minutes, 45 minutes, and 60 minutes were also significantly lower than those of the LPS group (all p < 0.001). Concentrations of p38 MAPK of the LPS+V group that harvested at 15 minutes, 30 minutes, and 45 minutes, but not at 60 minutes, were also significantly lower than those of the LPS group (all p < 0.001). In addition, immunohistochemistry assay revealed that the AP-1 fluorescence signals of the LPS+V group were weaker than those of the LPS group. Conclusion Vasopressin inhibits MAPKs and AP-1 in endotoxin-activated macrophages.",
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AU - Chen, Yu Long

AU - Chang, Ya Ying

AU - Kao, Ming Chang

AU - Huang, Chun Jen

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N2 - Objectives We have previously shown that vasopressin could inhibit the upregulation of inflammatory mediators. Expression of inflammatory mediators is tightly regulated by the upstream transcriptional pathway mitogen-activated protein kinases (MAPKs) and activated protein-1 (AP-1). In this study, we elucidated whether vasopressin could inhibit the upregulation of MAPKs/AP-1. Methods Murine macrophages (RAW264.7 cells) randomly received lipopolysaccharide (LPS; 100 ng/mL) or LPS plus vasopressin (1000 pg/mL) (designated as the LPS and the LPS+V groups, respectively). Control groups were run simultaneously. For MAPKs, cells were harvested at 0 minutes, 15 minutes, 30 minutes, 45 minutes, and 60 minutes after reaction. For AP-1, cells were harvested at 60 minutes after reaction. Between-group differences in MAPKs (i.e., extracellular regulated kinase, c-Jun N-terminal kinase, and p38 MAPK) and AP-1 expressions were compared. Results Immunoblotting assay data revealed that extracellular regulated kinase concentrations of the LPS +V group that harvested at 45 minutes and 60 minutes, but not at 15 minutes and 30 minutes, were significantly lower than those of the LPS group (p = 0.005 and p = 0.013). C-Jun N-terminal kinase concentrations of the LPS+V group that harvested at 15 minutes, 30 minutes, 45 minutes, and 60 minutes were also significantly lower than those of the LPS group (all p < 0.001). Concentrations of p38 MAPK of the LPS+V group that harvested at 15 minutes, 30 minutes, and 45 minutes, but not at 60 minutes, were also significantly lower than those of the LPS group (all p < 0.001). In addition, immunohistochemistry assay revealed that the AP-1 fluorescence signals of the LPS+V group were weaker than those of the LPS group. Conclusion Vasopressin inhibits MAPKs and AP-1 in endotoxin-activated macrophages.

AB - Objectives We have previously shown that vasopressin could inhibit the upregulation of inflammatory mediators. Expression of inflammatory mediators is tightly regulated by the upstream transcriptional pathway mitogen-activated protein kinases (MAPKs) and activated protein-1 (AP-1). In this study, we elucidated whether vasopressin could inhibit the upregulation of MAPKs/AP-1. Methods Murine macrophages (RAW264.7 cells) randomly received lipopolysaccharide (LPS; 100 ng/mL) or LPS plus vasopressin (1000 pg/mL) (designated as the LPS and the LPS+V groups, respectively). Control groups were run simultaneously. For MAPKs, cells were harvested at 0 minutes, 15 minutes, 30 minutes, 45 minutes, and 60 minutes after reaction. For AP-1, cells were harvested at 60 minutes after reaction. Between-group differences in MAPKs (i.e., extracellular regulated kinase, c-Jun N-terminal kinase, and p38 MAPK) and AP-1 expressions were compared. Results Immunoblotting assay data revealed that extracellular regulated kinase concentrations of the LPS +V group that harvested at 45 minutes and 60 minutes, but not at 15 minutes and 30 minutes, were significantly lower than those of the LPS group (p = 0.005 and p = 0.013). C-Jun N-terminal kinase concentrations of the LPS+V group that harvested at 15 minutes, 30 minutes, 45 minutes, and 60 minutes were also significantly lower than those of the LPS group (all p < 0.001). Concentrations of p38 MAPK of the LPS+V group that harvested at 15 minutes, 30 minutes, and 45 minutes, but not at 60 minutes, were also significantly lower than those of the LPS group (all p < 0.001). In addition, immunohistochemistry assay revealed that the AP-1 fluorescence signals of the LPS+V group were weaker than those of the LPS group. Conclusion Vasopressin inhibits MAPKs and AP-1 in endotoxin-activated macrophages.

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KW - p38 mitogen-activated protein kinase

KW - RAW264.7 cells

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