Comparative toxicity of fatty acids on a macrophage cell line (J774)

2006 ◽  
Vol 111 (5) ◽  
pp. 307-317 ◽  
Author(s):  
Thais Martins de Lima ◽  
Maria Fernanda Cury-Boaventura ◽  
Gisele Giannocco ◽  
Maria Tereza Nunes ◽  
Rui Curi
Keyword(s):  
Fatty Acids ◽  
Cell Death ◽  
Cell Line ◽  
Lipid Accumulation ◽  
Membrane Integrity ◽  
Peroxisome Proliferator ◽  
Macrophage Cell Line ◽  
Macrophage Cell ◽  
Peroxisome Proliferator Activated Receptor ◽  
High Concentrations

In the present study, the cytotoxicity of palmitic, stearic, oleic, linoleic, arachidonic, docosahexaenoic and eicosapentaenoic acids on a macrophage cell line (J774) was investigated. The induction of toxicity was investigated by changes in cell size, granularity, membrane integrity, DNA fragmentation and phosphatidylserine externalization by using flow cytometry. Fluorescence microscopy was used to determine the type of cell death (Acridine Orange/ethidium bromide assay). The possible mechanisms involved were examined by measuring mitochondrial depolarization, lipid accumulation and PPARγ (peroxisome-proliferator-activated receptor γ) activation. The results demonstrate that fatty acids induce apoptosis and necrosis of J774 cells. At high concentrations, fatty acids cause macrophage death mainly by necrosis. The cytotoxicity of the fatty acids was not strictly related to the number of double bonds in the molecules: palmitic acid>docosahexaenoic acid>stearic acid=eicosapentaenoic acid=arachidonic acid>oleic acid>linoleic acid. The induction of cell death did not involve PPARγ activation. The mechanisms of fatty acids to induce cell death involved changes in mitochondrial transmembrane potential and intracellular neutral lipid accumulation. Fatty acids poorly incorporated into triacylglycerol had the highest toxicity.

scholarly journals Prolonged survival but ultimate cell death of the rainbow trout macrophage cell line, RTS11, under different starvation regimens

2016 ◽  
Vol 53 ◽  
pp. 118
Author(s):  
Phuc H. Pham ◽  
Jun-Wen Li ◽  
Dustin Ammendolia ◽  
Patrick G. Pumputis ◽  
Lucy E.J. Lee ◽  
...  
Keyword(s):  
Cell Death ◽  
Rainbow Trout ◽  
Cell Line ◽  
Prolonged Survival ◽  
Macrophage Cell Line ◽  
Macrophage Cell

scholarly journals Staurosporine from Streptomyces sanyensis activates Programmed Cell Death in Acanthamoeba via the mitochondrial pathway and presents low in vitro cytotoxicity levels in a macrophage cell line

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Luis Cartuche ◽  
Ines Sifaoui ◽  
Darío Cruz ◽  
María Reyes-Batlle ◽  
Atteneri López-Arencibia ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Cell Line ◽  
Mitochondrial Pathway ◽  
In Vitro Cytotoxicity ◽  
Macrophage Cell Line ◽  
Macrophage Cell

Abstract 912: Spleen Tyrosine Kinase Regulates TLR4 dependent Macropinocytosis And Lipid Accumulation In Macrophages

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Soo-Ho Choi ◽  
Felicidad Almazan ◽  
Yury I Miller
Keyword(s):  
Tyrosine Kinase ◽  
Cell Line ◽  
Lipid Accumulation ◽  
Actin Polymerization ◽  
Foam Cell ◽  
Cell Formation ◽  
Foam Cell Formation ◽  
Macrophage Cell Line ◽  
Spleen Tyrosine Kinase ◽  
Macrophage Cell

Toll-like receptors play a key role in the signaling pathways of innate immune response and have been recently shown to contribute to vascular inflammation and atherosclerosis. Oxidation of LDL is considered a leading mechanism of atherogenesis, and in our previous studies, we demonstrated that minimally modified LDL (mmLDL) induced TLR4-dependent chemokine secretion as well as robust actin polymerization and spreading of macrophages. We noticed that these mmLDL-induced cytoskeletal rearrangements led to extensive vacuolization, characteristic of macropinocytosis. In this study, we examined the mechanisms of TLR4-induced actin polymerization and macropinocytosis. It has been reported that spleen tyrosine kinase (Syk) regulates actin cytoskeleton and that it may interact with TLR4. We found in the immunoprecipitation experiments that mmLDL induced Syk association with TLR4 as well as Syk phosphorylation. Next we developed a J774 macrophage cell line, which stably expressed Syk shRNA and had the Syk expression reduced by 70% or more. Using this Syk-deficient macrophage cell line and specific Syk inhibitors, we demonstrated that Syk is necessary for mmLDL-induced activation of Ras and phosphorylation of Raf-MEK1-ERK1/2. The ERK1/2 activation resulted in phosphorylation of paxillin and an increase in the formation of N-WASP/Arp2 complex, which initiates actin polymerization. Taken together, these results suggest that Syk is a critical kinase in the mmLDL macrophage activation and that the mmLDL-induced cytoskeleton signaling. In addition, we demonstrated that mmLDL induced macrophage uptake of native LDL and of fluorescent 10 KDa dextran, and that this effect was Syk-dependent. These data suggest a novel pathway for the mmLDL-induced macropinocytosis in macrophages, which may constitute a mechanism for macrophage lipid accumulation and foam cell formation, a characteristic step in the development of atherosclerosis.

Streptomyces spores from mouldy houses induce nitric oxide, TNFα and IL-6 secretion from RAW264.7 macrophage cell line without causing subsequent cell death

1997 ◽  
Vol 3 (1) ◽  
pp. 57-63 ◽  
Author(s):  
Maija-Riitta Hirvonen ◽  
Aino Nevalainen ◽  
Niina Makkonen ◽  
Jukka Mönkkönen ◽  
Kai Savolainen
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Cell Line ◽  
Macrophage Cell Line ◽  
Macrophage Cell ◽  
Raw264.7 Macrophage

Immune Enhancing Effect of Medicinal Herb Extracts on a RAW 264.7 Macrophage Cell Line

2012 ◽  
Vol 41 (11) ◽  
pp. 1521-1527 ◽  
Author(s):  
A-Reum Yu ◽  
Ho-Young Park ◽  
In-Wook Choi ◽  
Yong-Kon Park ◽  
Hee-Do Hong ◽  
...  
Keyword(s):  
Cell Line ◽  
Medicinal Herb ◽  
Raw 264.7 ◽  
Macrophage Cell Line ◽  
Macrophage Cell ◽  
Enhancing Effect ◽  
Raw 264.7 Macrophage ◽  
Herb Extracts
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