Prostacyclin induction by high-density lipoprotein (HDL) in vascular smooth muscle cells depends on sphingosine 1-phosphate receptors: effect of simvastatin.

@article{GonzlezDez2008ProstacyclinIB,
  title={Prostacyclin induction by high-density lipoprotein (HDL) in vascular smooth muscle cells depends on sphingosine 1-phosphate receptors: effect of simvastatin.},
  author={Mar{\'i}a Gonz{\'a}lez-D{\'i}ez and Cristina Rodr{\'i}guez and Lina Badim{\'o}n and Jos{\'e} Mart{\'i}nez-Gonz{\'a}lez},
  journal={Thrombosis and haemostasis},
  year={2008},
  volume={100 1},
  pages={
          119-26
        }
}
Prostacyclin (PGI2) is an important regulator of vascular homeostasis. Our goal was to analyze the role of sphingosine 1-phosphate (S1P) and its receptors in the up-regulation of cyclooxygenase-2 (Cox-2) induced by HDL in human vascular smooth muscle cells (VSMC). S1P induces Cox-2 expression in a time-and dose-dependent manner at concentrations (0.02-1 microM) compatible with those present in physiological HDL levels. The effect was mimicked by dihydro-S1P (DhS1P), a S1P derivative that only… 
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48 Citations
Highly Influential Citations
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Background Citations
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Results Citations
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48 Citations

High-density lipoprotein induces cyclooxygenase-2 expression and prostaglandin I-2 release in endothelial cells through sphingosine kinase-2
TLDR
Results indicate that HDL induces COX-2 expression and PGI-2 release in endothelial cells through activation of PKC, ERK1/2, and SphK-2 pathways, which implicate a novel mechanism underlying anti-atherothrombotic effects of HDL.
Sphingosine-1-phosphate: A bioactive lipid that confers high-density lipoprotein with vasculoprotection mediated by nitric oxide and prostacyclin.
TLDR
This review is focused on the central role of S1P as a bioactive component that confers vasculoprotective properties to HDL by eliciting a wide range of biological responses on endothelial and smooth muscle cells largely dependent on the up-regulation of NO and prostacyclin.
An involvement of SR-B1 mediated PI3K-Akt-eNOS signaling in HDL-induced cyclooxygenase 2 expression and prostacyclin production in endothelial cells.
Human apolipoprotein A-I induces cyclooxygenase-2 expression and prostaglandin I-2 release in endothelial cells through ATP-binding cassette transporter A1.
TLDR
The results indicate that apoA-I induces COX-2 expression and PGI-2 release through ABCA1 and the activation of intracellular p38 MAPK, ERK1/2, as well as JAK2 pathways, and apo-I can reinforce these effects with S1P in HUVECs, which could in part mediate antiatherogenic effects of HDL.
Sphingosine kinase inhibition exerts both pro- and anti-atherogenic effects in low-density lipoprotein receptor-deficient (LDL-R(-/-)) mice.
TLDR
Treatment with SphK inhibitor leads to both pro- and anti-atherogenic effects in LDL-R(-/-) mice, and SphK inhibition fails to affect atherosclerosis despite significant S1P reduction in plasma.
Cellular function and signaling pathways of vascular smooth muscle cells modulated by sphingosine 1-phosphate.
Simvastatin-induced sphingosine 1−phosphate receptor 1 expression is KLF2-dependent in human lung endothelial cells
TLDR
Simvastatin upregulates S1 PR1 transcription and expression via the transcription factor KLF2, and consequently augments the effects of S1PR1 agonists on preserving vascular barrier integrity, which may lead to novel combinatorial therapeutic strategies for lung inflammatory syndromes.
Targeting sphingosine-1-phosphate signalling for cardioprotection.
Cyclooxygenase-2 expression, prostacyclin production and endothelial protection of high-density lipoprotein.
TLDR
The roles of COx-2 as well as PGI2 in atherosclerosis and atherothrombosis, the controversial vascular effects on prostanoid inhibition by COX-2 inhibitors, and the effects of HDL on the endothelial protection by the upregulation of COX -2 and the release of PGI-2 during the progression of Atherosclerosis are summarized.
Sphingosine-1-phosphate as a mediator of high-density lipoprotein effects in cardiovascular protection.
TLDR
The potential benefits and limitations of S1P analogues as a new class of functional HDL mimetics for cardiovascular therapy are elucidated and the functional properties of 'free', HDL-unbound S 1P are sometimes different from or even contrary to those of HDL-associated S1p.
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