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smooth/triacylglycerol
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Metabolism of cytoplasmic triacylglycerol in cultured aortic smooth muscle cells.
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A turnover of cytoplasmic triacylglycerol was studied in cultured rat, rabbit, and bovine aortic smooth muscle cells. Cytoplasmic triacylglycerol was labeled with [3H]glycerol in the presence of oleic acid in the medium and its loss from the cell was studied in the presence of carrier glycerol.
Effect of TNF on triacylglycerol in cultured vascular smooth muscle cells.
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Smooth muscle cells (SMC) isolated from bovine aorta or human saphenous vein were cultured and used to study the putative effect of recombinant human tumor necrosis factor (TNF) on lipid metabolism in vascular cells. Addition of TNF to the culture medium for 24-48 h resulted in an increase of
Comparison of fatty acid and triacylglycerol metabolism of macrophages and smooth muscle cells.
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The response of macrophages and smooth muscle cells to culture in free fatty acid has been compared. Because oleate and linoleate promoted triacylglycerol enrichment of smooth muscle cells, whereas palmitate had little effect, oleate was used for these studies. The kinetics of the accumulation of
Macrophage interaction with very-low-density lipoproteins results in triacylglycerol-enriched smooth muscle cells.
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Macrophage-conditioned medium containing very-low-density lipoproteins (VLDL) and its effects on smooth muscle cell triacylglycerol metabolism was investigated. Macrophages exposed to VLDL from normolipemic rats accumulated high levels of intracellular triacylglycerol, while similarly treated smooth
Metabolic fate of exogenous diacylglycerols in A10 smooth muscle cells.
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The metabolic fate of exogenous diacylglycerols, 1-palmitoyl-2-[1-14C]oleoyl-sn-glycerol (2-[14C]POG) and 1-stearoyl-2-[1-14C]arachidonoyl-sn-glycerol (2-[14C]SAG), was determined after incubation of A10 smooth muscle cells with liposomal suspensions. Hydrolysis through a diacylglycerol (DG) lipase
Signal transduction in vascular smooth muscle: diacylglycerol second messengers and PKC action.
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Agonist-stimulated phospholipid turnover can generate diacylglycerol (DAG), an intracellular second messenger that activates protein kinase C (PKC). DAG can be produced from the hydrolysis of phosphatidylinositol 4,5-bisphosphate (PIP2) by a phosphoinositide-specific phospholipase C and by the
Adipocytic differentiation and liver x receptor pathways regulate the accumulation of triacylglycerols in human vascular smooth muscle cells.
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Lipid accumulation by vascular smooth muscle cells (VSMC) is a feature of atherosclerotic plaques. In this study we describe two mechanisms whereby human VSMC foam cell formation is driven by de novo synthesis of fatty acids leading to triacylglycerol accumulation in intracellular vacuoles, a
Eicosapentaenoic acid and docosahexaenoic acid suppress the proliferation of vascular smooth muscle cells.
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Eicosapentaenoic acid, which is one of the n-3 polyunsaturated fatty acids (PUFA), is reported to exert its antithrombotic and anti-atherogenic effect partly through the modulation of vascular cell functions. Vascular smooth muscle cell (VSMC) proliferation plays an important role in the
Diacylglycerols derived from membrane phospholipids are metabolized by lipases in A10 smooth muscle cells.
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The metabolic fate of endogenous diacylglycerol (DAG) in cultured A10 smooth muscle cells was determined. Preincubation of A10 cells with [3H]myristic acid or [3H]arachidonic acid resulted in preferential labeling of phosphatidylcholine (PC) or phosphatidylinositol (PI), respectively. Addition of
Uptake of chylomicron remnants causes cholesterol accumulation in cultured human arterial smooth muscle cells.
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Chylomicron remnants (Sf greater than 100) were prepared by treating human chylomicrons (Sf greater than 400) with human post heparin plasma. Chylomicron remnants recovered after 70-80% of chylomicron triacylglycerol was hydrolyzed, suppressed LDL-receptor activity and increased cell cholesterol
Vascular smooth muscle function in type 2 diabetes mellitus: a systematic review and meta-analysis.
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OBJECTIVE
In type 2 diabetes, in contrast to the well-documented endothelial dysfunction, studies assessing vascular smooth muscle (VSM) function have yielded discrepant results over the last two decades. We therefore sought to determine whether or not VSM function is impaired in individuals with
Molecular motions and thermotropic phase behavior of triacylglycerols and cholesteryl esters in herpesvirus-infected arterial smooth muscle cells: a deuterium nuclear magnetic resonance study.
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The physical state of lipids in arterial smooth muscle cells (SMC) may contribute to lipid accumulation following injury. We have previously demonstrated that herpes simplex virus (HSV) infection alters the physical state of the neutral lipid accumulating in arterial SMC, as determined by
Long-chain acyl-CoA synthetase 4 modulates prostaglandin E₂ release from human arterial smooth muscle cells.
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Long-chain acyl-CoA synthetases (ACSLs) catalyze the thioesterification of long-chain FAs into their acyl-CoA derivatives. Purified ACSL4 is an arachidonic acid (20:4)-preferring ACSL isoform, and ACSL4 is therefore a probable regulator of lipid mediator production in intact cells. Eicosanoids play
Oxysterol mediated changes in fatty acid distribution and lipid synthesis in cultured bovine aortic smooth muscle cells.
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We studied the actions of oxysterols on fatty acid distribution and lipid synthesis in cultured bovine aortic smooth muscle cells. Cultures were labeled with [1-14C]arachidonate or [1-14C]oleate. During a 24-hr incubation, 25- or 22R-hydroxycholesterol enhanced the incorporation of label into
Mechanisms of enhanced production of PGI2 in cultured rat vascular smooth muscle cells enriched with eicosapentaenoic acid.
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The present investigation was performed to clarify the effect of EPA on PGI2 production in vitro using cultured rat vascular smooth muscle cells (VSMC). To simulate in vivo conditions, a triacylglycerol (TG) emulsified form of EPA was used. An increase in EPA content was achieved without alteration
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