Lipid metabolism in human endothelial cells

Héliès-Toussaint, Cécile; Gambert, Ségolène; Roller, Pauline; Tricot, Sabine; Lacour, Bernard; Grynberg, Alain

doi:10.1016/j.bbalip.2006.05.013

Cited by 20 publications

(24 citation statements)

References 35 publications

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“…60,61 Saturated and unsaturated fatty acids are incorporated into endothelial cell phospholipids in different periods of time. 60 This fact may be important for the effect of FA on cell function. Thus studies on the effect of fatty acids on membrane phospholipids synthesis in lymphocytes should be now performed.…”

Section: Discussionmentioning

confidence: 99%

Regulation of human lymphocyte proliferation by fatty acids

Gorjão

Cury-Boaventura

Lima

et al. 2006

Cell Biochemistry & Function

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In the present study, the effect of increasing concentrations of palmitic (PA, C16:0), stearic (SA, C18:0), oleic (OA, C18:1, n-9), linoleic (LA, C18:2n-6), docosahexaenoic (DHA, C22:6 n-3) and eicosapentaenoic (EPA, C20:5 n-3) acids on lymphocyte proliferation was investigated. The maximal non-toxic concentrations of these fatty acids for human lymphocytes in vitro were determined. It was also evaluated whether these fatty acids at non-toxic concentrations affect IL-2 induced lymphocyte proliferation and cell cycle progression. OA and LA at 25 microM increased lymphocyte proliferation and at higher concentrations (75 microM and 100 microM) inhibited it. Both fatty acids promoted cell death at 200 microM concentration. PA and SA decreased lymphocyte proliferation at 50 microM and promoted cell death at concentrations of 100 microM and above. EPA and DHA decreased lymphocyte proliferation at 25 and 50 microM being toxic at 50 and 100 microM, respectively. PA, SA, DHA and EPA decreased the stimulatory effect of IL-2 on lymphocyte proliferation, increasing the percentage of cells in G1 phase and decreasing the proportion of cells in S and G2/M phases. OA and LA caused an even greater pronounced effect. The treatment with all fatty acids increased neutral lipid accumulation in the cells but the effect was more pronounced with PA and DHA. In conclusion, PA, SA, DHA and EPA decreased lymphocyte proliferation, whereas OA and LA stimulated it at non-toxic concentrations.

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Section: Discussionmentioning

confidence: 99%

Regulation of human lymphocyte proliferation by fatty acids

Gorjão

Cury-Boaventura

Lima

et al. 2006

Cell Biochemistry & Function

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“…Depending on concentration, they disturb plasma membranes 12 or remove certain lipids from the membranes. 29 Lipid constitution varies between cell types, 30 thus Caco-2 cell membrane lipid composition 31 differs from endothelial ones, 32 and lipid rafts are also dissimilar. 30 Differences in the membrane lipid composition and in lipid rafts of endothelial and epithelial cells may be related to our observations on the divergent effects of Chremophors on these cell types.…”

Section: Discussionmentioning

confidence: 99%

Kinetic Analysis of the Toxicity of Pharmaceutical Excipients Cremophor EL and RH40 on Endothelial and Epithelial Cells

Kiss

Walter

Bocsik

et al. 2013

Journal of Pharmaceutical Sciences

100

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“…; Helies‐Toussaint et al. ). We recently reported that supplementation of culture medium with a low, but pharmacologically relevant, concentration of niacin (10 μ mol/L) improves human microvascular endothelial cell tube formation during exposure to excess palmitate under normoxic conditions (Hughes‐Large et al.…”

Section: Introductionmentioning

confidence: 99%

“…Uptake and accumulation of surplus fatty acids (particularly saturated species) from both lipoprotein-derived and albumin-bound sources can lead to cell dysfunction and cell damage, a process referred to as lipotoxicity, in cells and tissues throughout the body including those of the vasculature (Kim et al 2012;Wende et al 2012;Symons and Abel 2013). Endothelial cells may be especially vulnerable to lipotoxicity because, despite being continually exposed to elevated circulating lipids and lipids within steatotic tissues during obesity and metabolic syndrome, they are not metabolically programmed to process large quantities of fatty acids (Dagher et al 2001;Helies-Toussaint et al 2006). We recently reported that supplementation of culture medium with a low, but pharmacologically relevant, concentration of niacin (10 lmol/L) improves human microvascular endothelial cell tube formation during exposure to excess palmitate under normoxic conditions (Hughes-Large et al 2014).…”

Section: Introductionmentioning

confidence: 99%

Niacin promotes revascularization and recovery of limb function in diet‐induced obese mice with peripheral ischemia

Pang

Zhang

Sutherland

et al. 2016

Pharmacology Res & Perspec

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Niacin can reduce vascular disease risk in individuals with metabolic syndrome, but in light of recent large randomized controlled trials outcomes, its biological actions and clinical utility remain controversial. Niacin can improve endothelial function, vascular inflammation, and vascular regeneration, independent of correcting dyslipidemia, in various lean rodent models of vascular injury. Here, we tested whether niacin could directly improve endothelial cell angiogenic function during combined exposure to excess fatty acids and hypoxia, and whether intervention with niacin during continued feeding of western diet could improve revascularization and functional recovery in obese, hyperlipidemic mice with peripheral ischemia. Treatment with niacin (10 μmol/L) increased human microvascular endothelial cell angiogenic function during exposure to high fatty acids and hypoxia (2% oxygen), as determined by tube formation on Matrigel. To assess revascularization in vivo, we used western diet‐induced obese mice with unilateral hind limb femoral artery ligation and excision. Treatment for 14 days postinjury with once daily i.p. injections of a low dose of niacin (50 mg/kg) improved recovery of hind limb use, in association with enhanced revascularization and decreased inflammation of the tibialis anterior muscle. These effects were concomitant with decreased plasma triglycerides, but not increased plasma apoAI. Thus, niacin improves endothelial tube formation under lipotoxic and hypoxic conditions, and moreover, promotes revascularization and functional hind limb recovery following ischemic injury in diet‐induced obese mice with hyperlipidemia. These data may have implications for niacin therapy in the treatment of peripheral ischemic vascular disease associated with metabolic syndrome.

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Lipid metabolism in human endothelial cells

Cited by 20 publications

References 35 publications

Regulation of human lymphocyte proliferation by fatty acids

Regulation of human lymphocyte proliferation by fatty acids

Kinetic Analysis of the Toxicity of Pharmaceutical Excipients Cremophor EL and RH40 on Endothelial and Epithelial Cells

Niacin promotes revascularization and recovery of limb function in diet‐induced obese mice with peripheral ischemia

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