Lipid droplets formation in human endothelial cells in response to polyunsaturated fatty acids and 1-methyl-nicotinamide (MNA); confocal Raman imaging and fluorescence microscopy studies

2015 ◽  
Vol 9 (4) ◽  
pp. 396-405 ◽  
Author(s):  
Katarzyna Majzner ◽  
Stefan Chlopicki ◽  
Malgorzata Baranska
Keyword(s):  
Fatty Acids ◽  
Endothelial Cells ◽  
Fluorescence Microscopy ◽  
Polyunsaturated Fatty Acids ◽  
Lipid Droplets ◽  
Raman Imaging ◽  
Human Endothelial Cells ◽  
Confocal Raman

scholarly journals Selective internalization of arachidonic acid by endothelial cells

1987 ◽  
Vol 245 (1) ◽  
pp. 151-157 ◽  
Author(s):  
E R Hall ◽  
C E Manner ◽  
J Carinhas ◽  
R Snopko ◽  
M Rafelson
Keyword(s):  
Fatty Acids ◽  
Endothelial Cells ◽  
Arachidonic Acid ◽  
Endothelial Cell ◽  
Polyunsaturated Fatty Acids ◽  
Cell Types ◽  
Time Dependent ◽  
Asymmetric Distribution ◽  
Membrane Phospholipids ◽  
Bovine Endothelial Cell

The asymmetric distribution of phospholipids in bovine endothelial-cell membranes was probed with 2,4,6-trinitrobenzenesulphonate and purified phospholipase A2. The data suggest that phosphotidylethanolamine is primarily located in the inner lipid bilayer, as reported for other cell types. Stearic acid is taken up by the endothelial cells and is randomly distributed among the membrane phospholipids. In contrast, the polyunsaturated fatty acids (arachidonic, eicosatrienoic and eicosapentaenoic acids) have initial incorporation into the phosphatidylcholine fraction. These fatty acids then undergo a time-dependent transfer from phosphatidylcholine to phosphatidylethanolamine. Thus we propose that endothelial cells possess a mechanism for the selective internalization of polyunsaturated fatty acids.

scholarly journals Impact of Polyunsaturated Fatty Acids on miRNA Profiles of Monocytes/Macrophages and Endothelial Cells—A Pilot Study

2017 ◽  
Vol 18 (2) ◽  
pp. 284 ◽  
Author(s):  
Claudia Roessler ◽  
Kevin Kuhlmann ◽  
Christine Hellwing ◽  
Anja Leimert ◽  
Julia Schumann
Keyword(s):  
Fatty Acids ◽  
Endothelial Cells ◽  
Pilot Study ◽  
Polyunsaturated Fatty Acids

Cholesterol and ω-3 fatty acids inhibit Na, K-ATPase activity in human endothelial cells

1999 ◽  
Vol 142 (2) ◽  
pp. 327-333 ◽  
Author(s):  
Vincent Mayol ◽  
Marie-Josée Duran ◽  
Alain Gerbi ◽  
Françoise Dignat-George ◽  
Samuel Lévy ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Endothelial Cells ◽  
Atpase Activity ◽  
Human Endothelial Cells

scholarly journals Effect of docosahexaenoic acid plus insulin on atherosclerotic human endothelial cells

2020 ◽  
Author(s):  
Aysan Eslami Abriz ◽  
Reza Rahbarghazi ◽  
Alireza Nourazarian ◽  
Çıgır Biray Avci ◽  
Soltan Ali Mahboob ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Endothelial Cells ◽  
Docosahexaenoic Acid ◽  
Palmitic Acid ◽  
Pcr Array ◽  
Omega 3 Fatty Acids ◽  
Omega 3 ◽  
Human Endothelial Cells ◽  
Array Analysis ◽  
Tnf Α

Abstract Background: Atherosclerosis is touted as one of the most critical consequences of diabetes mellitus indicated by local inflammation of endothelial cells. The Effect of Omega 3 fatty acids, mainly docosahexaenoic acid (DHA), has been investigated in cells after exposure to high doses of lipids. The current experiment aimed to address the modulatory effects of docosahexaenoic acid and insulin in palmitic-treated human endothelial cells. Methods: Human umbilical vein endothelial cells were treated with 1mM palmitic acid, 50μM insulin, 50μM docosahexaenoic acid, and their combination for 48 hours. Cell survival rate and apoptosis were measured using MTT and flow cytometry assays. The Griess assay detected NO levels. Protein levels of TNF-α, IL-6, and NF-κB were studied using ELISA and immunofluorescence imaging. The expression of genes participating in atherosclerosis was monitored using PCR array analysis. Results: Oil Red O staining showed the inhibitory effect of DHA and insulin to reduce the intracellular accumulation of palmitic acid. Both DHA and Insulin blunted palmitic acid detrimental effects on HUVECs indicated by an increased survival rate (p<0.05). The percent of apoptotic cells was decreased in palmitic-treated cells received insulin and DHA compared to palmitic-treated group (p<0.05). Based on our data, DHA and Insulin diminished the production of all inflammatory cytokines, TNF-α, IL-6, and NF-κB, in palmitic-treated cells (p<0.05). Similar to these data, NO production was also decreased in all groups treated with insulin and DHA compared to the palmitic-treated cells (p<0.05). PCR array analysis revealed the modulatory effect of DHA and insulin on the expression of atherosclerosis-related genes pre-treated with palmitic acid compared to the control group (p<0.05). Conclusion: DHA and Insulin could alter the dynamic growth and dysfunctional activity of human endothelial cells after treatment with palmitic acid. Taken together, Omega 3 fatty acids, along with insulin, could dictate specific cell behavior in endothelial cells in vitro

The Effect of Polyunsaturated Fatty Acids on Endothelial Cells and Their Production of Prostacyclin, Thromboxane and Platelet Inhibitory Activity

1983 ◽  
Vol 50 (04) ◽  
pp. 762-767 ◽  
Author(s):  
Jan H Brox ◽  
Arne Nordøy
Keyword(s):  
Fatty Acids ◽  
Endothelial Cells ◽  
Arachidonic Acid ◽  
Endothelial Cell ◽  
Polyunsaturated Fatty Acids ◽  
Linolenic Acid ◽  
Inhibitory Activity ◽  
Primary Cultures ◽  
Cell Monolayers ◽  
Docosahexaenoic Acids

SummaryPrimary cultures of human endothelial cell monolayers were incubated with albumin-bound fatty acids of the ω-3 and ω-6 families for a maximum of 24 hrs, to investigate the production of 6-keto-PGF1α, TXB2 and platelet inhibitory activity (PIA). Arachidonic acid was a potent stimulator of all parameters. The release of 6-keto-PGF1α was significantly reduced by equimolar concentrations of linoleic, dihomogamma linolenic and eicosapentaenoic acids, but not by linolenic acid. PIA was not similarity affected.Dihomogamma linolenic add was also a weak stimulator of 6- keto-PGF1α and PIA, but reduced the content of both in the cells after 24 hrs. Eicosapentaenoic and docosahexaenoic acids both depressed 6-keto-PGF1α production but PIA was maintained after 24 hrs. Indomethacin always blocked 6-keto-PGF1α and PIA production. None of the effects correlated to release of 51CR from prelabelled cells.

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