High-fat/high-cholesterol diet promotes a S1P receptor-mediated antiapoptotic activity for VLDL

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

doi:10.1194/jlr.m600201-jlr200

Cited by 8 publications

(8 citation statements)

References 31 publications

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“…Recent evidence also supports the role of S1P transported in HDL in modifying multiple cellular metabolic pathways via its binding to one or more of the receptors in the S1P family of receptors (42)(43)(44)(45)(46)(47)(48). However, the mechanism whereby HDL-associated S1P can signal through S1P receptors is not well understood.…”

Section: Discussionmentioning

confidence: 99%

HDL3, but not HDL2, stimulates plasminogen activator inhibitor-1 release from adipocytes: the role of sphingosine-1-phosphate

Lee

Hammad

Semler

et al. 2010

Journal of Lipid Research

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Section: Discussionmentioning

confidence: 99%

HDL3, but not HDL2, stimulates plasminogen activator inhibitor-1 release from adipocytes: the role of sphingosine-1-phosphate

Lee

Hammad

Semler

et al. 2010

Journal of Lipid Research

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“…However, VLDL isolated from mice fed a high-fat/ high-cholesterol/cholate diet inhibits caspase 3/7 activation (60). This high-fat diet VLDL-related anti-caspase activity can be blocked by treatment with the S1P receptor antagonist VPC 23019 or by S1P3-specific small interfering RNA (60).…”

Section: Hdl-s1p Stimulates Endothelial Cell Growth and Survivalmentioning

confidence: 99%

“…Evidence for this conclusion comes from the findings that suppression of Akt activity by wortmannin and LY-294002 or by a dominant negative Akt eliminates the antiapoptotic effects of SPC and LSF on endothelial cells (e.g., these treatments prevented the activation of caspase 9 and 3) (59). By contrast to HDL, VLDL isolated from mice on a regular chow diet provides little apoptosis protection to endothelial cells (60). However, VLDL isolated from mice fed a high-fat/ high-cholesterol/cholate diet inhibits caspase 3/7 activation (60).…”

Section: Hdl-s1p Stimulates Endothelial Cell Growth and Survivalmentioning

confidence: 99%

HDL serves as a S1P signaling platform mediating a multitude of cardiovascular effects

Argraves

2007

Journal of Lipid Research

134

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The lysosphingolipid sphingosine 1-phosphate (S1P) is a component of HDL. Findings from a growing number of studies indicate that S1P is a mediator of many of the cardiovascular effects of HDL, including the ability to promote vasodilation, vasoconstriction, and angiogenesis, protect against ischemia/reperfusion injury, and inhibit/ reverse atherosclerosis. These latter cardioprotective effects are being shown to involve the S1P-mediated suppression of inflammatory processes, including reduction of the endothelial expression of monocyte and lymphocyte adhesion molecules, decreased recruitment of polymorphonuclear cells to sites of infarction, and blocking of cardiomyocyte apoptosis after myocardial infarction. This review article summarizes the evidence that S1P as a component of HDL serves to regulate vascular cell and lymphocyte behaviors associated with cardiovascular (patho)physiology. (1) were the first to show that the lysosphingolipid sphingosine 1-phosphate (S1P) was a component of human plasma, present at a concentration of ?200 nM. After these findings were published, Sachinidis et al. (2) reported that human LDL and HDL possess a signaling activity that promoted extracellular signal-regulated protein kinase phosphorylation in a pertussis toxin-sensitive manner. HPLC fractionation of plasma LDL and HDL showed that the lipoproteinassociated signaling activity had a chromatographic elution profile corresponding to that of purified S1P. Further evidence appeared demonstrating that ?65% of the S1P in blood is associated with the lipoproteins LDL, VLDL, and HDL, with the bulk of lipoprotein-associated S1P (?54%) bound to HDL (3). Measurements of the S1P content of human HDL and LDL particles show that these lipoproteins contain ?180 and 70 pmol S1P/mg protein, respectively (4). Together, these findings have set the stage for investigations into the mechanism of S1P incorporation into lipoproteins and the physiological significance of lipoproteins as carriers of S1P, and the findings of these investigations are summarized in this review.

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“…Lipoproteins were isolated from human plasma as described previously (59)(60)(61). Blood (60 ml) from fed or fasted individuals was collected in the presence of EDTA (3.2 mM), chloramphenicol (80 μg/ml), sodium azide (0.1 mg/ml), gentamicin (80 μg/ml), and protease inhibitors (Complete Protease Inhibitor Cocktail tablets, Roche Applied Science) and centrifuged at 1,500 g (average g) for 10 minutes at 4°C.…”

Section: Methodsmentioning

confidence: 99%

Immunoglobulin-like domain containing receptor 1 mediates fat-stimulated cholecystokinin secretion

Chandra

Wang²,

Shahid³

et al. 2013

J. Clin. Invest.

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Cholecystokinin (CCK) is a satiety hormone produced by discrete enteroendocrine cells scattered among absorptive cells of the small intestine. CCK is released into blood following a meal; however, the mechanisms inducing hormone secretion are largely unknown. Ingested fat is the major stimulant of CCK secretion. We recently identified a novel member of the lipoprotein remnant receptor family known as immunoglobulinlike domain containing receptor 1 (ILDR1) in intestinal CCK cells and postulated that this receptor conveyed the signal for fat-stimulated CCK secretion. In the intestine, ILDR1 is expressed exclusively in CCK cells. Orogastric administration of fatty acids elevated blood levels of CCK in wild-type mice but not Ildr1-deficient mice, although the CCK secretory response to trypsin inhibitor was retained. The uptake of fluorescently labeled lipoproteins in ILDR1-transfected CHO cells and release of CCK from isolated intestinal cells required a unique combination of fatty acid plus HDL. CCK secretion secondary to ILDR1 activation was associated with increased [Ca 2+ ] i , consistent with regulated hormone release. These findings demonstrate that ILDR1 regulates CCK release through a mechanism dependent on fatty acids and lipoproteins and that absorbed fatty acids regulate gastrointestinal hormone secretion.

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High-fat/high-cholesterol diet promotes a S1P receptor-mediated antiapoptotic activity for VLDL

Cited by 8 publications

References 31 publications

HDL3, but not HDL2, stimulates plasminogen activator inhibitor-1 release from adipocytes: the role of sphingosine-1-phosphate

HDL3, but not HDL2, stimulates plasminogen activator inhibitor-1 release from adipocytes: the role of sphingosine-1-phosphate

HDL serves as a S1P signaling platform mediating a multitude of cardiovascular effects

Immunoglobulin-like domain containing receptor 1 mediates fat-stimulated cholecystokinin secretion

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