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J. Lipid Res.
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A more recent version of this article appeared on April 1, 2007

Papers In Press, published online ahead of print January 30, 2007
J. Lipid Res., doi:10.1194/jlr.M600201-JLR200
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Submitted on May 9, 2006
Revised on January 25, 2007
Accepted on January 29, 2007

High fat/ high cholesterol diet promotes an S1P receptor-mediated anti-apoptotic activity for VLDL

Mirta Mihovilovic, Jennifer B. Robinette, Robert M. DeKroon, Patrick M. Sullivan, and Warren J. Strittmatter

Medicine/Division of Neurology, Duke University Medical Center, Durham, NC 27710

Corresponding Author: mihov001{at}mc.duke.edu

Withdrawing growth factors or serum from endothelial cells leads to the activation of effector caspases 3 and 7 resulting in apoptotic cell death. HDL protects against caspase induction through sphingosine-1-phosphate (S1P) receptors. This anti-caspase activity of HDL is antagonized by VLDL from apolipoprotein E4 (genotype: APOE4/4; apolipoprotein: apoE) targeted replacement (TR) mice, but not by VLDL from TR APOE3/3 mice, and requires binding of apoE4-VLDL to an LDL receptor family member. In the absence of HDL, apoE4-VLDL and apoE3-VLDL from TR mice have limited anti-apoptotic activity. In contrast, we show here that a high fat/high cholesterol/cholate diet (HFD) radically alters this biological activity of VLDL. On HFD, both apoE3-VLDL and apoE4-VLDL (HFD VLDL) inhibit caspase 3/7 activation initiated by serum withdrawal. This activity of HFD VLDL is independent of an LDL receptor family member but requires activation of S1P3 receptors, as shown by the ability of pharmacological block of S1P receptors by VPC 23019 and by siRNA-mediated down regulation of S1P3 receptors to inhibit HFD VLDL anti-caspase activity.


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K. M. Argraves and W. S. Argraves
HDL serves as a S1P signaling platform mediating a multitude of cardiovascular effects
J. Lipid Res., November 1, 2007; 48(11): 2325 - 2333.
[Abstract] [Full Text] [PDF]


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