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

Wang BW, Lin CM, Wu GJ, Shyu KG - J. Biomed. Sci. (2011)

Bottom Line: Visfatin, a adipocytokine with insulin-mimetic effect, plays a role in endothelial angiogenesis.However, the molecular mechanism of beneficial effects of HBO is poorly understood.HBO significantly increased secretion of TNF-α from cultured human CAECs.

View Article: PubMed Central - HTML - PubMed

Affiliation: Division of Cardiology, Shin Kong Wu Ho-Su Memorial Hospital, and School of Medicine, Fu-Jen Catholic University, New Taipei City, Taipei, Taiwan.

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-α 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-α from cultured human CAECs. Exogenous addition of TNF-α significantly increased visfatin protein expression while TNF-α antibody and TNF-α 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-α antibody attenuated the glucose uptake induced by HBO. HBO significantly increased the tube formation of human CAECs while visfatin siRNA, TNF-α antibody inhibited the tube formation induced by HBO.

Conclusions: HBO activates visfatin expression in cultured human CAECs. HBO-induced visfatin is mediated by TNF-α and at least in part through JNK pathway.

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Effect of HBO on human CAECs tube formation. A, Representative image of tube formation of human CAECs. B, Quantitative tube length measurement (n = 5). *P < 0.001 vs. HBO alone.
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Figure 8: Effect of HBO on human CAECs tube formation. A, Representative image of tube formation of human CAECs. B, Quantitative tube length measurement (n = 5). *P < 0.001 vs. HBO alone.

Mentions: To test the effect of HBO on the function of human CAECs, tube formation and migration activity was examined. As shown in Figure 8, HBO for 6 h significantly increased the tube formation of human CAECs. Pretreatment with SP600125, TNF-α monoclonal antibody, and visfatin siRNA significantly blocked the induction of tube formation by HBO. The control siRNA did not inhibit the tube formation induced by HBO. HBO for 6 h significantly increased the migration activity of human CAECs (Figure 9). Pretreatment with SP600125, TNF-α monoclonal antibody, and visfatin siRNA significantly blocked the induction of migration by HBO. The control siRNA did not inhibit the migration induced by HBO.


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

Wang BW, Lin CM, Wu GJ, Shyu KG - J. Biomed. Sci. (2011)

Effect of HBO on human CAECs tube formation. A, Representative image of tube formation of human CAECs. B, Quantitative tube length measurement (n = 5). *P < 0.001 vs. HBO alone.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3113732&req=5

Figure 8: Effect of HBO on human CAECs tube formation. A, Representative image of tube formation of human CAECs. B, Quantitative tube length measurement (n = 5). *P < 0.001 vs. HBO alone.
Mentions: To test the effect of HBO on the function of human CAECs, tube formation and migration activity was examined. As shown in Figure 8, HBO for 6 h significantly increased the tube formation of human CAECs. Pretreatment with SP600125, TNF-α monoclonal antibody, and visfatin siRNA significantly blocked the induction of tube formation by HBO. The control siRNA did not inhibit the tube formation induced by HBO. HBO for 6 h significantly increased the migration activity of human CAECs (Figure 9). Pretreatment with SP600125, TNF-α monoclonal antibody, and visfatin siRNA significantly blocked the induction of migration by HBO. The control siRNA did not inhibit the migration induced by HBO.

Bottom Line: Visfatin, a adipocytokine with insulin-mimetic effect, plays a role in endothelial angiogenesis.However, the molecular mechanism of beneficial effects of HBO is poorly understood.HBO significantly increased secretion of TNF-α from cultured human CAECs.

View Article: PubMed Central - HTML - PubMed

Affiliation: Division of Cardiology, Shin Kong Wu Ho-Su Memorial Hospital, and School of Medicine, Fu-Jen Catholic University, New Taipei City, Taipei, Taiwan.

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-α 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-α from cultured human CAECs. Exogenous addition of TNF-α significantly increased visfatin protein expression while TNF-α antibody and TNF-α 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-α antibody attenuated the glucose uptake induced by HBO. HBO significantly increased the tube formation of human CAECs while visfatin siRNA, TNF-α antibody inhibited the tube formation induced by HBO.

Conclusions: HBO activates visfatin expression in cultured human CAECs. HBO-induced visfatin is mediated by TNF-α and at least in part through JNK pathway.

Show MeSH
Related in: MedlinePlus