- 作者: Bao-Wei Wang; Chiu-Mei Lin; Gong-Jhe Wu; Kou-Gi Shyu
- 作者服務機構: School of Medicine, Fu-Jen Catholic University, New Taipei City, Taiwan, R.O.C.
- 中文摘要: --
- 英文摘要:
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. - 中文關鍵字: --
- 英文關鍵字: --