Tumor necrosis factor-enhances hyperbaric oxygen-induced visfatin expression via JNK pathway in human coronary arterial endothelial cells

Bao Wei Wang, Chiu Mei Lin, Gong-Jhe Wu, Kou-Gi Shyu

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Background: Visfatin, a adipocytokine with insulin-mimetic effect, plays a role in endothelial angiogenesis. Hyperbaric oxygen (HBO) has been used in medical practice. However, the molecular mechanism of beneficial effects of HBO is poorly understood. We sought to investigate the cellular and molecular mechanisms of regulation of visfatin by HBO in human coronary arterial endothelial cells (CAECs). Methods. Human CAECs were exposed to 2.5 atmosphere absolute (ATA) of oxygen in a hyperbaric chamber. Western blot, real-time polymerase chain reaction, and promoter activity assay were performed. In vitro glucose uptake and tube formation was detected. Results: Visfatin protein (2.55-fold) and mRNA (2.53-fold) expression were significantly increased after exposure to 2.5 ATA HBO for 4 to 6 h. Addition of SP600125 and JNK siRNA 30 min before HBO inhibited the induction of visfatin protein. HBO also significantly increased DNA-protein binding activity of AP-1 and visfatin promoter activity. Addition of SP600125 and TNF- monoclonal antibody 30 min before HBO abolished the DNA-protein binding activity and visfatin promoter activity induced by HBO. HBO significantly increased secretion of TNF- from cultured human CAECs. Exogenous addition of TNF- significantly increased visfatin protein expression while TNF- antibody and TNF- receptor antibody blocked the induction of visfatin protein expression induced by HBO. HBO increased glucose uptake in human CAECs as HBO and visfatin siRNA and TNF- antibody attenuated the glucose uptake induced by HBO. HBO significantly increased the tube formation of human CAECs while visfatin siRNA, TNF- antibody inhibited the tube formation induced by HBO. Conclusions: HBO activates visfatin expression in cultured human CAECs. HBO-induced visfatin is mediated by TNF- and at least in part through JNK pathway.

Original languageEnglish
Article number27
JournalJournal of Biomedical Science
Volume18
Issue number1
DOIs
Publication statusPublished - 2011

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Nicotinamide Phosphoribosyltransferase
MAP Kinase Signaling System
Endothelial cells
Endothelial Cells
Tumor Necrosis Factor-alpha
Oxygen
Small Interfering RNA
Antibodies
DNA-Binding Proteins
Atmosphere
Glucose
Hyperbaric chambers
Proteins

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Molecular Biology
  • Cell Biology
  • Biochemistry, medical
  • Endocrinology, Diabetes and Metabolism
  • Pharmacology (medical)

Cite this

Tumor necrosis factor-enhances hyperbaric oxygen-induced visfatin expression via JNK pathway in human coronary arterial endothelial cells. / Wang, Bao Wei; Lin, Chiu Mei; Wu, Gong-Jhe; Shyu, Kou-Gi.

In: Journal of Biomedical Science, Vol. 18, No. 1, 27, 2011.

Research output: Contribution to journalArticle

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abstract = "Background: Visfatin, a adipocytokine with insulin-mimetic effect, plays a role in endothelial angiogenesis. Hyperbaric oxygen (HBO) has been used in medical practice. However, the molecular mechanism of beneficial effects of HBO is poorly understood. We sought to investigate the cellular and molecular mechanisms of regulation of visfatin by HBO in human coronary arterial endothelial cells (CAECs). Methods. Human CAECs were exposed to 2.5 atmosphere absolute (ATA) of oxygen in a hyperbaric chamber. Western blot, real-time polymerase chain reaction, and promoter activity assay were performed. In vitro glucose uptake and tube formation was detected. Results: Visfatin protein (2.55-fold) and mRNA (2.53-fold) expression were significantly increased after exposure to 2.5 ATA HBO for 4 to 6 h. Addition of SP600125 and JNK siRNA 30 min before HBO inhibited the induction of visfatin protein. HBO also significantly increased DNA-protein binding activity of AP-1 and visfatin promoter activity. Addition of SP600125 and TNF- monoclonal antibody 30 min before HBO abolished the DNA-protein binding activity and visfatin promoter activity induced by HBO. HBO significantly increased secretion of TNF- from cultured human CAECs. Exogenous addition of TNF- significantly increased visfatin protein expression while TNF- antibody and TNF- receptor antibody blocked the induction of visfatin protein expression induced by HBO. HBO increased glucose uptake in human CAECs as HBO and visfatin siRNA and TNF- antibody attenuated the glucose uptake induced by HBO. HBO significantly increased the tube formation of human CAECs while visfatin siRNA, TNF- antibody inhibited the tube formation induced by HBO. Conclusions: HBO activates visfatin expression in cultured human CAECs. HBO-induced visfatin is mediated by TNF- and at least in part through JNK pathway.",
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N2 - Background: Visfatin, a adipocytokine with insulin-mimetic effect, plays a role in endothelial angiogenesis. Hyperbaric oxygen (HBO) has been used in medical practice. However, the molecular mechanism of beneficial effects of HBO is poorly understood. We sought to investigate the cellular and molecular mechanisms of regulation of visfatin by HBO in human coronary arterial endothelial cells (CAECs). Methods. Human CAECs were exposed to 2.5 atmosphere absolute (ATA) of oxygen in a hyperbaric chamber. Western blot, real-time polymerase chain reaction, and promoter activity assay were performed. In vitro glucose uptake and tube formation was detected. Results: Visfatin protein (2.55-fold) and mRNA (2.53-fold) expression were significantly increased after exposure to 2.5 ATA HBO for 4 to 6 h. Addition of SP600125 and JNK siRNA 30 min before HBO inhibited the induction of visfatin protein. HBO also significantly increased DNA-protein binding activity of AP-1 and visfatin promoter activity. Addition of SP600125 and TNF- monoclonal antibody 30 min before HBO abolished the DNA-protein binding activity and visfatin promoter activity induced by HBO. HBO significantly increased secretion of TNF- from cultured human CAECs. Exogenous addition of TNF- significantly increased visfatin protein expression while TNF- antibody and TNF- receptor antibody blocked the induction of visfatin protein expression induced by HBO. HBO increased glucose uptake in human CAECs as HBO and visfatin siRNA and TNF- antibody attenuated the glucose uptake induced by HBO. HBO significantly increased the tube formation of human CAECs while visfatin siRNA, TNF- antibody inhibited the tube formation induced by HBO. Conclusions: HBO activates visfatin expression in cultured human CAECs. HBO-induced visfatin is mediated by TNF- and at least in part through JNK pathway.

AB - Background: Visfatin, a adipocytokine with insulin-mimetic effect, plays a role in endothelial angiogenesis. Hyperbaric oxygen (HBO) has been used in medical practice. However, the molecular mechanism of beneficial effects of HBO is poorly understood. We sought to investigate the cellular and molecular mechanisms of regulation of visfatin by HBO in human coronary arterial endothelial cells (CAECs). Methods. Human CAECs were exposed to 2.5 atmosphere absolute (ATA) of oxygen in a hyperbaric chamber. Western blot, real-time polymerase chain reaction, and promoter activity assay were performed. In vitro glucose uptake and tube formation was detected. Results: Visfatin protein (2.55-fold) and mRNA (2.53-fold) expression were significantly increased after exposure to 2.5 ATA HBO for 4 to 6 h. Addition of SP600125 and JNK siRNA 30 min before HBO inhibited the induction of visfatin protein. HBO also significantly increased DNA-protein binding activity of AP-1 and visfatin promoter activity. Addition of SP600125 and TNF- monoclonal antibody 30 min before HBO abolished the DNA-protein binding activity and visfatin promoter activity induced by HBO. HBO significantly increased secretion of TNF- from cultured human CAECs. Exogenous addition of TNF- significantly increased visfatin protein expression while TNF- antibody and TNF- receptor antibody blocked the induction of visfatin protein expression induced by HBO. HBO increased glucose uptake in human CAECs as HBO and visfatin siRNA and TNF- antibody attenuated the glucose uptake induced by HBO. HBO significantly increased the tube formation of human CAECs while visfatin siRNA, TNF- antibody inhibited the tube formation induced by HBO. Conclusions: HBO activates visfatin expression in cultured human CAECs. HBO-induced visfatin is mediated by TNF- and at least in part through JNK pathway.

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