Biomedical subjects

T L Kaduce

Publications and source records attributed to T L Kaduce.

At least 37 records · Page 2Linked to original sources

PubMed1993

14,15-Epoxyeicosatrienoic acid metabolism in endothelial cells.

Epoxyeicosatrienoic acid (EET) metabolism was studied in endothelial cells to determine whether this tissue may influence their vasoactive properties. Porcine aortic endothelial cells rapidly took up all four EET regioisomers. The uptake of [1-14C]14,15-EET reached a maximum in 15-30 min, and saturation was not observed with concentrations up to 5 microM. More than 70% of the incorporated 14,15-EET was contained in choline and inositol glycerophospholipids, most of it in the form of an EET ester. A metabolite, 14,15-dihydroxyeicosatrienoic acid (14,15-DHET), accumulated in the medium during incubation, and products with similar chromatographic properties also were formed from 5,6-, 8,9-, and 11,12-EET. Much of the 14,15-EET taken up was only temporarily retained by the cells, and in 2 h half was released into the medium as 14,15-DHET. Bovine aortic and human umbilical vein endothelial cells also took up 14,15-EET, incorporated it into choline glycerophospholipids, and converted it to 14,15-DHET. These findings suggest that the endothelium may limit the vascular actions of EETs through rapid uptake, hydration, and release of DHETs into the circulation. Some vasoactive effects of EETs may result from their temporary accumulation in endothelial phospholipids involved in stimulus-response coupling.

8,11,14-Eicosatrienoic Acid↗

PubMed1992

Myristic acid utilization in Chinese hamster ovary cells and peroxisome-deficient mutants.

Chinese hamster ovary (CHO) cells convert [9,10-3H]myristic acid ([3H]14:0) to several lipid-soluble, radioactive metabolites that are released into the medium. The main products are lauric (12:0) and decanoic (10:0) acids. Some of the 12:0 formed also is retained in cell lipids. Similar metabolites are not synthesized from palmitic (16:0), oleic (18:1), or arachidonic (20:4) acids, and the addition of these fatty acids does not reduce the conversion of [3H]14:0 to 12:0. Two peroxisome-deficient CHO cell lines do not convert [3H] 14:0 to any polar metabolites, but, they elongate, desaturate, and incorporate [3H]14:0 into intracellular lipids and proteins normally. While BC3H1 muscle cells convert some [3H]14:0 to 12:0, they also produce at least nine lipid-soluble polar products from [3H]12:0. These findings suggest that a previously unrecognized function of myristic acid is to serve as a substrate for the synthesis of 12:0, which can be either secreted into the medium or converted to other oxidized metabolites. The absence of this peroxisomal oxidation pathway, however, does not interfere with other aspects of myristic acid metabolism, including protein myristoylation.

Animals↗

PubMed1991

Myristic acid utilization and processing in BC3H1 muscle cells.

Because myristic acid (14:0) is important in regulating cell function, we have studied its utilization in BC3H1 muscle cells. Phosphatidylcholine contained 70-80% of the [9,10-3H]14:0 radioactivity incorporated into the cell phospholipids. In both myoblasts and myocytes, however, large amounts of radioactivity also accumulated in a labile neutral lipid pool consisting mostly of triacylglycerol. Therefore, radioactive lipid products formed when BC3H1 cells labeled with 14:0 are stimulated are not necessarily derived only from phosphatidylcholine. Elongation of [9,10-3H]14:0 occurred rapidly in the myoblasts and myocytes, and extensive desaturation also occurred in the myoblasts. Thus, even after short periods of labeling, substantial amounts of radioactivity are contained in fatty acids other than 14:0. The labeling of proteins with [9,10-3H]myristic acid was generally similar in the myoblasts and myocytes. A number of lipid-soluble, polar radioactive metabolites were released into the medium during incubation of [9,10-3H]14:0 with the cells. [1-14C] 14:0 was not converted to these compounds, indicating that they are chain-shortened 14:0 derivatives. Based on chemical analysis, two of the major products appear to be hydroxylated fatty acids. This oxidation process shows some specificity for 14:0 because similar compounds were not produced from palmitic, oleic, or linoleic acids. The myocytes formed larger amounts of the metabolites than the myoblasts, suggesting that differentiation may increase the activity of this 14:0 oxidative pathway.

Acylation↗

PubMed1990

Localization of 12-hydroxyeicosatetraenoic acid in endothelial cells.

Bovine aortic endothelial cells take up 12-hydroxyeicosatetraenoic acid (12-HETE), a lipoxygenase product formed from arachidonic acid. The uptake of [3H]12-HETE reached a maximum in 2 to 4 h. At this time, from 75 to 80% of the incorporated radioactivity was contained in phospholipids, about 85% of the esterified radioactivity remained in the form of 12-HETE, and at least 90% of the phospholipid radioactivity was present in the sn-2-position. Subcellular fractionation on Percoll and sucrose gradients demonstrated that 65 to 74% of the radioactivity was present in membranes enriched in NADPH-cytochrome c reductase and UDP-galactosyl transferase. The specific radioactivity relative to protein of these intracellular membranes was 2.9-times higher than in a plasma membrane fraction enriched in 5'-nucleotidase. A similar intracellular localization was observed when [3H]5-HETE or [3H]arachidonic acid were taken up. The 12-HETE was contained primarily in the choline glycerophospholipids of the microsomal membranes. After incorporation, [3H]12-HETE was removed from the cell lipids much more rapidly than [3H]arachidonic acid, and 80% of the radioactivity released into the medium during the first hour remained as 12-HETE. Because it accumulates in microsomal membranes, 12-HETE uptake may perturb certain intracellular processes and thereby lead to endothelial dysfunction. The relatively rapid removal of the newly incorporated 12-HETE may be an important protective mechanism that prevents excessive accumulation and more extensive endothelial damage.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗

PubMed1989

Formation of 9-hydroxyoctadecadienoic acid from linoleic acid in endothelial cells.

Human umbilical vein endothelial cells convert linoleic acid to two monohydroxyoctadecadienoic (HODE) acids, 9- and 13-HODE. More 9-HODE than 13-HODE is formed under most conditions. The production of these metabolites is reduced substantially by acetylsalicylic acid, ibuprofen, or arachidonic acid, suggesting that cyclooxygenase may be involved in endothelial HODE synthesis. Incubations lasting up to 4 h indicate that the endothelial cells can convert [U-14C] linoleic acid into at least four additional products, some of which may be derived from the HODE that is formed initially. Radioactive 9- and 13-HODE are produced when the endothelial cells are labeled with linoleic acid and then exposed to thrombin, suggesting that these metabolites also may be formed when the endothelium is activated. If endothelial monolayers grown on micropore filters are incubated with linoleic acid, a substantial amount of the HODE formed accumulates in the basolateral fluid. This suggests that HODE may have extracellular effects, especially within the vascular wall. Furthermore, when 9- or 13-HODE are added, endothelial cultures produce less prostaglandin I2 and convert less 12-hydroxyeicosatetraenoic acid to its main metabolite, 8-hydroxyhexadecatrienoic acid. Therefore, in addition to extracellular actions, HODE also may have functional effects within the endothelium.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗

PubMed1988

Conversion of 15-hydroxyeicosatetraenoic acid to 11-hydroxyhexadecatrienoic acid by endothelial cells.

Cultured endothelial cells take up 15-hydroxyeicosatetraenoic acid (15-HETE), a lipoxygenase product formed from arachidonic acid, and incorporate it into cellular phospholipids and glycerides. Uptake can occur from either the apical or basolateral surface. A substantial amount of the 15-HETE incorporated into phospholipids is present in the inositol phosphoglycerides. 15-HETE is converted into several metabolic products that accumulate in teh extracellular fluid; this conversion does not require stimulation by agonists. The main product has been identified as 11-hydroxyhexadecatrienoic acid [16:3(11-OH)], a metabolite of 15-HETE that has not been described previously. Formation of 16:3(11-OH) decreases when 4-pentenoic acid is present, suggesting that it is produced by beta-oxidation. The endothelial cells can take up 16:3(11-OH) only 25% as effectively as 15-HETE, and 16:3(11-OH) is almost entirely excluded from the inositol phosphoglycerides. These results suggest that the endothelial cells can incorporate 15-HETE when it is released into their environment. Through partial oxidation, the endothelium can process 15-HETE to a novel metabolite that is less effectively taken up and, in particular, is excluded from the inositol phosphoglycerides.

Animals↗

PubMed1987

Formation of 8-hydroxyhexadecatrienoic acid by vascular smooth muscle cells.

Smooth muscle cells derived from the human umbilical vein produce four radioactive metabolites when they are incubated in culture with [3H]-12-hydroxyeicosatetraenoic acid. This conversion does not require the addition of an agonist for eicosanoid formation. The main product, which accounts for 60% of the radioactivity converted to these metabolites, has been identified as 8-hydroxyhexadecatrienoic acid.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗

PubMed1986

Composition and incorporation of [3H]arachidonic acid into molecular species of phospholipid classes by cultured human endothelial cells.

Based on quantitative high-performance liquid chromatographic analyses of molecular species in selected phospholipid subclasses from culture human umbilical vein endothelial cells, the relative degree of unsaturation was ethanolamine plasmalogens greater than phosphatidylethanolamine greater than phosphatidylcholine. A total of 36 different molecular species were identified in the phosphatidylcholine fraction. Interestingly, the phosphatidylcholine contained a significant amount (11.7%) of the dipalmitoyl species, a lipid normally associated with lung surfactant. The arachidonoyl-containing molecular species of phosphatidylserine/inositol were labeled to the highest extent and the ethanolamine plasmalogens contained the lowest specific radioactivity after incubating [3H]arachidonic acid with human endothelial cells for 4 h. Within each phospholipid subclass the arachidonoyl species where both acyl groups of the phospholipid are unsaturated (20:4-20:4, 18:2-20:4 + 16:1-20:4, and 18:1-20:4) had higher specific radioactivities, after labeling with [3H]arachidonic acid, than those that contained saturated aliphatic chains (16:0-20:4 and 18:0-20:4). This indicates that the unsaturated species have higher turnover rates.

Arachidonic Acid↗

PubMed1986

Metabolism of platelet activating factor (1-alkyl-2-acetyl-sn-glycero-3-phosphocholine) and 1-alkyl-2-acetyl-sn-glycerol by human endothelial cells.

The metabolism of platelet activating factor (1-[1,2-3H]alkyl-2-acetyl-sn-glycero-3-phosphocholine) and 1-[1,2-3H]alkyl-2-acetyl-sn-glycerol was studied in cultures of human umbilical vein endothelial cells. Human endothelial cells deacetylated 1-[1,2-3H]alkyl-2-acetyl-sn-glycero-3-phosphocholine to the corresponding lyso compound (1-[1,2-3H]alkyl-2-lyso-sn-glycerol-3-phosphocholine) and a portion was converted to 1-[1,2-3H]alkyl-2-acyl(long-chain)-sn-glycero-3-phosphocholine. Lyso platelet activating factor (lyso-PAF) (1-[1,2-3H]alkyl-2-lyso-sn-glycero-3-phosphocholine) was detected in the media very early during the incubation and the amount remained higher than the level of the lyso product observed in the cells. Cellular levels of 1-[1,2-3H]alkyl-2-lyso-sn-glycero-3-phosphocholine were significantly higher than the acylated product (1-[1,2-3H]alkyl-2-acyl(long-chain)-sn-glycero-3-phosphocholine) at all times during the 60-min incubation period, which suggests that the ratio of acetylhydrolase to acyltransferase activities is greater in endothelial cells than in most other cells. When endothelial cells were incubated with 1-[1,2-3H]alkyl-2-acetyl-sn-glycerol, a known precursor of PAF, 1-[1,2-3H]alkyl-sn-glycerol was the major metabolite formed (greater than 95% of the 3H-labeled metabolites during 20- and 40-min incubations). At least a portion of the acetate was removed from 1-[1,2-3H]alkyl-2-acetyl-sn-glycerol by a hydrolytic factor released from the endothelial cells into the medium during the incubations. Only negligible amounts of the total cellular radioactivity (0.2%) was incorporated into platelet activating factor (1-[1,2-3H]alkyl-2-acetyl-sn-glycero-3-phosphocholine); therefore, it is unlikely that the previously observed hypotensive activity of 1-alkyl-2-acetyl-sn-glycerols can be explained on the basis of the conversion to platelet activating factor (1-alkyl-2-acetyl-sn-glycero-3-phosphocholine) by endothelial cells. Results of this investigation indicate that endothelial cells play an important role in PAF catabolism. Undoubtedly, the endothelium is important in the regulation of PAF levels in the vascular system.

Animals↗

PubMed1986

Eicosapentaenoic acid utilization by bovine aortic endothelial cells: effects on prostacyclin production.

We have investigated whether the presence of other fatty acids in physiologic amounts will influence the effects of eicosapentaenoic acid on cellular lipid metabolism and prostaglandin production. Eicosapentaenoic acid uptake by cultured bovine aortic endothelial cells was time and concentration dependent. At concentrations between 1 and 25 microM, most of the eicosapentaenoic acid was incorporated into phospholipids and of this, 60-90% was present in choline phosphoglycerides. Eicosapentaenoic acid inhibited arachidonic acid uptake and conversion to prostacyclin (prostaglandin I2) but was not itself converted to eicosanoids. Only small effects on the uptake of 10 microM eicosapentaenoic acid occurred when palmitic, stearic or oleic acids were added to the medium in concentrations up to 75 microM. In contrast, eicosapentaenoic acid uptake was reduced considerably by the presence of linoleic, n-6 eicosatrienoic, arachidonic or docosahexaenoic acids. Although a 100 microM mixture of palmitic, stearic, oleic and linoleic acid (25:10:50:15) had little effect on the uptake of 10 or 20 microM eicosapentaenoic acid, less of this acid was channeled into endothelial phospholipids. However, the fatty acid mixture did not prevent the inhibitory effect of eicosapentaenoic acid on prostaglandin I2 formation in response to either arachidonic acid or ionophore A23187. An 8 h exposure to eicosapentaenoic acid was required for the inhibition to become appreciable and, after 16 h, prostaglandin I2 production was reduced by as much as 60%. These findings indicate that the capacity of aortic endothelial cells to produce prostaglandin I2 is decreased by continuous exposure to eicosapentaenoic acid. Even if the eicosapentaenoic acid is present as a small percentage of a physiologic fatty acid mixture, it is still readily incorporated into endothelial phospholipids and retains its inhibitory effect against endothelial prostaglandin I2 formation. Therefore, these actions may be representative of the in vivo effects of eicosapentaenoic acid on the endothelium.

6-Ketoprostaglandin F1 alpha↗

PubMed1986

Docosatetraenoic acid in endothelial cells: formation, retroconversion to arachidonic acid, and effect on prostacyclin production.

Cultured bovine aortic endothelial cells convert arachidonic acid to docosatetraenoic acid and also take up docosatetraenoic acid from the extracellular fluid. After a 24-h incubation with biosynthetically prepared [3H]docosatetraenoic acid, about 20% of the cellular fatty acid radioactivity was converted to arachidonic acid. Furthermore, in pulse-chase experiments, the decrease in phospholipid docosatetraenoic acid content was accompanied by an increase in arachidonic acid, providing additional evidence for retroconversion. These findings suggest that one possible function of docosatetraenoic acid in endothelial cells is to serve as a source of arachidonic acid. The endothelial cells can release docosatetraenoic acid when they are stimulated with ionophore A23187, but they do not form appreciable amounts of eicosanoids from docosatetraenoic acid. Enrichment of the endothelial cells with docosatetraenoic acid reduced their capacity to produce prostacyclin (PGI2) in response to ionophore A23187. This may be related to the fact that docosatetraenoic acid enrichment caused a 40% reduction in the arachidonic acid content of the inositol phosphoglycerides. In addition, less prostacyclin was formed when the enriched cells were incubated with arachidonic acid, suggesting that docosatetraenoic acid also may act as an inhibitor of prostaglandin synthesis in endothelial cells.

Animals↗

PubMed1986

Free fatty acid release from endothelial cells.

Cultured bovine aortic endothelial cells that have been previously enriched with fatty acid are able to release free fatty acid (FFA) into the extracellular fluid. No stimulus other than the presence of albumin in the medium is needed to elicit the FFA release. Intracellular triglycerides appear to be the source of most of the FFA that is released. The released FFA is composed of a mixture of fatty acids, with the fatty acid used to enrich the cells contributing about half of the total. Under certain conditions sufficient fatty acid can be released to increase the FFA concentration of the extracellular fluid. Cells enriched initially with arachidonic acid released 1.7- to 2.9-times more FFA as compared to cells enriched with corresponding amounts of oleic acid. Neither prostaglandins nor lipoxygenase products contributed appreciably to the amount of FFA released from cells enriched with arachidonic acid. Porcine pulmonary artery endothelial cells also can release net amounts of FFA. These findings indicate that endothelial cells have the capacity to release fatty acid in the form of FFA. This process could possibly play a role in the transfer of fatty acids, particularly arachidonic acid, across the endothelium.

Animals↗

PubMed1985

Morphological alterations in cultured endothelial cells induced by arachidonic acid.

The addition of arachidonic acid (20:4), but not other fatty acids, including the structurally similar eicosapentaenoic acid (20:5), induced specific morphological changes in cultured endothelial cells derived from bovine aorta and pulmonary artery. Cells exhibited a time- and dose-dependent change from their normal, epithelioid morphology to become elongated, polygonal, and spindle-shaped. Cells isolated from aorta appeared more sensitive to these changes than those from pulmonary artery. The effect was observed as early as 12 h after exposure to 20:4, required 48 h for maximal expression, and could be reversed in 2-5 h after change to normal media. The morphological alteration was not observed in cells treated with leukotrienes or PGE2. When cells were pretreated with ibuprofen, aspirin, or indomethacin to block prostaglandin synthesis and then exposed to 20:4, the dose-response effect was shifted to the left. This increased sensitivity to 20:4 suggests either a direct effect of 20:4 on cell morphology or an indirect effect due to metabolites of 20:4 which are not dependent on the cyclooxygenase pathway.

Animals↗

PubMed1985

Effect of human plasma lipoproteins on prostacyclin production by cultured endothelial cells.

Prostacyclin (PGI2) production by bovine aortic or human umbilical vein endothelial cells increased when either human high density lipoproteins3 (HDL3) or low density lipoproteins (LDL) were added to a serum-free culture medium. At low concentrations and short incubation times, HDL3 produced more PGI2 than LDL, but LDL was just as effective as HDL3 in 18-hr incubations with high concentrations of lipoproteins. Neither lipoprotein was toxic to the cultures as assessed by [3H]leucine incorporation into cell protein. The stimulatory effect of HDL3 and LDL on PGI2 production decreased as growing cultures became confluent. Incubation with lipoproteins neither enhanced arachidonic acid release nor increased PGI2 formation when the cells were stimulated subsequently with ionophore A23187, indicating that the lipoproteins do not affect the intracellular processes involved in PGI2 production. The addition of albumin reduced the amount of PGI2 formation elicited by HDL3 or LDL. As compared with albumin-bound arachidonic acid, from 6- to 13-fold less PGI2 was produced during incubation with the lipoproteins. Furthermore, the amount of PGI2 formation elicited by the lipoproteins in 18 hr was 4-fold less than that produced during incubation with a fatty acid mixture containing only 5% arachidonic acid, and 3-fold less than when the cells were stimulated with the ionophore A23187 for 20 min. Taken together, our results indicate that human HDL and LDL contribute to endothelial PGI2 production only in a modest way and suggest that this process is not specific for either of these two plasma lipoproteins. In view of the greater participation of albumin-bound arachidonic acid in PGI2 production, plasma lipoproteins may not play as important a role in endothelial prostaglandin formation as has been suggested.

Animals↗

PubMed1985

A comparison of lipid metabolism in two human retinoblastoma cell lines.

A number of differences have been observed in the lipid metabolism of cultured Y79 and WERI Rb-1 retinoblastoma cells. The Y79 cells have a higher phospholipid content and a higher percentage of ethanolamine phosphoglycerides, whereas the WERI Rb-1 cells have more triglycerides. This is consistent with the finding that most of the polyunsaturated fatty acid taken up by the Y79 cells is incorporated into phospholipids, while a sizable amount of the uptake in WERI Rb-1 cells is incorporated into triglyceride. Polyunsaturated fatty acids of the n-6 class are taken up at about the same rate by both cells, but the n-3 polyunsaturates are taken up more rapidly by the Y79 cells. In addition, the Y79 cells convert a larger percentage of linoleic acid (18:2, n-6) to arachidonic acid (20:4, n-6) and of linolenic acid (18:3, n-3) to docosahexaenoic acid (22:6, n-3), and they accumulate these products when the precursors are added to the culture medium. When grown in 10% fetal bovine serum without supplemental fatty acid, however, the WERI Rb-1 contain more arachidonic and docosahexaenoic acids. These differences in lipid content and metabolism suggest that although the Y79 and WERI Rb-1 cell lines are derived from the same type of retinal tumor, they either originated from functionally different retinal neurons or have diverged biochemically during propagation in culture.

Cell Line↗

PubMed1984

Effects of membrane lipid unsaturation on the interactions of insulin and multiplication stimulating activity with endothelial cells.

Modification of plasma membrane fatty acyl composition has resulted in major changes in insulin binding and insulin action in several cell types. In the present study, endothelial cells, which in vivo are directly bathed by the changing fatty acid and insulin environment of the bloodstream, were grown in media enriched in specific saturated, monounsaturated and polyunsaturated fatty acids. These media conditions resulted in major and specific alteration in fatty acyl unsaturation of both neutral lipids and phospholipids of the endothelial cells. Despite the extensive fatty acyl changes, the lipid-modified cells demonstrated no change in the binding of insulin or the insulin-like growth factor, multiplication stimulating activity, and little alteration in insulin-induced down-regulation of the insulin receptor, or in cell processing of insulin. We suggest that the insulin receptor of the endothelial cell responds in a different manner than other cell types to similar alterations of membrane fatty acyl composition.

Animals↗

PubMed1983

Eicosapentaenoic acid and prostacyclin production by cultured human endothelial cells.

Human umbilical vein endothelial cells incorporate eicosapentaenoic acid (EPA) when this fatty acid is present in the culture medium. From 30 to 70% of the uptake remains as EPA, and much of the remainder is elongated to docosapentaenoic acid. All of the cellular glycerophospholipids become enriched with EPA and docosapentaenoic acid, with the largest increase in EPA occurring in the choline glycerophospholipids. When this fraction is enriched with EPA, it exhibits a large decrease in arachidonic acid content. Cultures exposed to tracer amounts of [1-14C]linolenic acid in 5% fetal bovine serum convert as much as 17% of the radioactivity to EPA. The conversion is reduced, however, in the presence of either 20% fetal bovine serum or 50 microM linolenic acid. Like arachidonic acid, some newly incorporated EPA was released from the endothelial cells when the cultures were exposed to thrombin. However, as compared with arachidonic acid, only very small amounts of EPA were converted to prostaglandins. Cultures enriched with EPA exhibited a 50 to 90% reduction in capacity to release prostacyclin (PGI2) when subsequently stimulated with thrombin, calcium ionophore A23187, or arachidonic acid. The degree of inhibition was dependent on the time of exposure to EPA and the EPA concentration, and it was not prevented by adding a reversible cyclooxygenase inhibitor, ibuprofen, during EPA supplementation. EPA appears to decrease the capacity of the endothelial cells to produce PGI2 in two ways: by reducing the arachidonic acid content of the cell phospholipid precursor pools and by acting as an inhibitor of prostaglandin production. These findings suggest that regimens designed to reduce platelet aggregation and thrombosis by EPA enrichment may also reduce the capacity of the endothelium to produce PGI2.

6-Ketoprostaglandin F1 alpha↗

PubMed1983

Role of triglycerides in endothelial cell arachidonic acid metabolism.

Arachidonic acid was incorporated into triglycerides by cultured bovine endothelial cells in a time- and concentration-dependent manner. At 75 microM or higher, more arachidonic acid was incorporated into triglycerides than into phospholipids. The triglyceride content of the cells increased as much as 5.5-fold, cytoplasmic inclusions appeared, and arachidonic acid comprised 22% of the triglyceride fatty acids. Triglyceride turnover occurred during subsequent maintenance culture; there was a 60% decrease in the radioactive arachidonic acid contained in triglycerides and a 40% decrease in triglyceride content in 6 hr. Most of the radioactivity was released into the medium as free fatty acid. The turnover of arachidonic acid, but not oleic acid in cellular triglycerides, decreased when supplemental fatty acid was added to the maintenance medium. Incorporation and turnover of radioactive arachidonic acid in triglycerides also was observed in human skin fibroblasts, 3T3-L1 cells, and MDCK cells. Other fatty acids were incorporated into triglycerides by the endothelial cells; the amounts after a 16-hr incubation with 50 microM fatty acid were 20:3 greater than 20:4 greater than 18:1 greater than 18:2 greater than 22:6 greater than 16:0 greater than 20:5. These findings indicate that triglyceride formation and turnover can play a role in the fatty acid metabolism of endothelial cells and that arachidonic acid can be stored in endothelial cell triglycerides.

Animals↗