scholarly journals Oxidized LDL Increases and Interferon-γ Decreases Expression of CD36 in Human Monocyte–Derived Macrophages

1998 ◽  
Vol 18 (8) ◽  
pp. 1350-1357 ◽  
Author(s):  
Tsutomu Nakagawa ◽  
Shuichi Nozaki ◽  
Makoto Nishida ◽  
Janabi Mohamed Yakub ◽  
Yoshiaki Tomiyama ◽  
...  
Keyword(s):  
Oxidized Ldl ◽  
Human Monocyte ◽  
Interferon Γ

Abstract 512: The Long Non-coding Rna MIAT Regulates Smooth Muscle Cell Proliferation and Macrophage Activity in Advanced Atherosclerotic Lesions

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Yuhuang Li ◽  
Hong Jin ◽  
Ljubica Perisic ◽  
Ekaterina Chernogubova ◽  
Alexandra Bäcklund ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Oxidized Ldl ◽  
In Silico Analysis ◽  
Human Monocyte ◽  
Carotid Plaques ◽  
Knock Down ◽  
Plaque Stability ◽  
Atherosclerotic Lesions ◽  
Markers Of Inflammation

Background: Long noncoding RNAs (lncRNAs) have emerged as critical epigenetic regulators in various biological processes and diseases. Here we sought to identify and functionally characterize the lncRNA MIAT as a novel regulator in atherosclerotic plaque stability. Methods and results: We profiled RNA transcript expression in patients with advanced atherosclerotic lesions from the Biobank of Karolinska Endarterectomies (BiKE). By microarray analysis, lncRNA MIAT was identified as one of the most highly up-regulated non-coding RNAs in carotid plaques compared to iliac artery controls, which was confirmed by qRT-PCR and in situ hybridization. Additional in silico analysis indicated a substantial positive correlation of MIAT with markers of inflammation, apoptosis and matrix degradation in carotid plaques. Experimental knock-down of MIAT, utilizing site-specific antisense oligonucleotides (LNA-GapmeRs) not only markedly decreased proliferation and migration rates of cultured human carotid artery smooth muscle cells (hCASMCs), but also increased their levels of apoptosis. In addition, MIAT inhibition significantly impaired oxidized LDL (oxLDL) uptake of murine peritoneal as well as human monocyte-differentiated macrophages in vitro. In contrast, induction of MIAT expression by lipoprotein-a (LPa) treatment, displayed the opposite effect. Conditioned medium from macrophage cultures after MIAT knock-down substantially decreased hCASMC proliferation, indicating a potential involvement of MIAT in macrophage-SMC interactions during advanced stages of atherosclerosis. Conclusion: The lncRNA MIAT is a novel regulator of cellular processes in atherosclerosis and plaque stability, which influences SMC proliferation and apoptosis and interacts with disease-triggering macrophages.

scholarly journals Treatment of macrophages with oxidized low-density lipoprotein increases their intracellular glutathione content

1991 ◽  
Vol 278 (2) ◽  
pp. 429-434 ◽  
Author(s):  
V M Darley-Usmar ◽  
A Severn ◽  
V J O'Leary ◽  
M Rogers
Keyword(s):  
Oxidized Ldl ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Human Monocyte ◽  
Cell Types ◽  
Oxidative Modification ◽  
Glutathione Depletion ◽  
Lipid Phase ◽  
Low Density ◽  
Oxidized Low Density Lipoprotein

Macrophages derived from the human monocyte cell line THP-1 or isolated from the peritoneum of C3H/HEJ mice were incubated with oxidized low-density lipoprotein (LDL) and the total glutathione content (oxidized plus reduced) was measured. An initial depletion of glutathione was followed by an increase, such that after a period of 24 h the glutathione content has approximately doubled. This response required the oxidation of the lipid phase of the LDL molecule, since both native LDL and acetylated LDL had little effect on glutathione levels. The response of the cells to oxidized LDL was dependent on the extent of oxidative modification of the protein. It was also found that 4-hydroxynonenal had a similar effect on THP-1 cells, and we suggest that this or other aldehydes present in oxidized LDL causes the induction of glutathione synthesis in response to an initial oxidative stress and consequent glutathione depletion. In addition, we found that both cell types possess transferases and peroxidases capable of detoxifying aldehydes and peroxides. However, treatment of cells with oxidized LDL or 4-hydroxynonenal for a period of 24 h had no effect on the activities of these enzymes.

Activation of Human Monocyte-Derived Macrophages Cultured on Teflon: Response to Interferon-γ during Terminal Maturation in vitro

Immunobiology ◽  
1988 ◽  
Vol 177 (2) ◽  
pp. 186-198 ◽  
Author(s):  
Reinhard Andreesen ◽  
Stephen Gadd ◽  
Wolfram Brugger ◽  
Georg W. Löhr ◽  
Robert C. Atkins
Keyword(s):  
Human Monocyte ◽  
Interferon Γ ◽  
Maturation In Vitro

Tryptophan Metabolites as Scavengers of Reactive Oxygen and Chlorine Species

Pteridines ◽  
2002 ◽  
Vol 13 (4) ◽  
pp. 140-143 ◽  
Author(s):  
Günter Weiss ◽  
Antonio Diez-Ruiz ◽  
Christian Murr ◽  
Igor Theur ◽  
Dietmar Fuchs
Keyword(s):  
Reactive Oxygen Species ◽  
Hydrogen Peroxide ◽  
Hypochlorous Acid ◽  
Reactive Oxygen ◽  
Human Monocyte ◽  
Interferon Γ ◽  
Oxygen Species ◽  
Tryptophan Degradation ◽  
Tryptophan Metabolites

Abstract Upon stimulation with interferon-γ, a typical Thl cell-derived cytokine, human monocyte-dertved macrophages produce neopterin derivatives and in parallel degrade the essential amino acid L-tryptophan to L-kynurenine and subsequently to 3-hydroxyanthramlic acid and anthramlic acid. In parallel, stimulated macrophages produce reactive oxygen species such as hydrogen peroxide and hypochlorous acid. Earlier, neopterin and 7.8-dihydroneoptenn were found to enhance or decrease effects of reactive oxygen species in vitro, depending on concentration and on environmental condition. In this study, we investigated the ability of tryptophan and its metabolites to interfere with radicals in vitro by means of a chemiluminiseence-based assay system. When using hydrogen peroxide or chloramine Τ as source for radical formation. L-tryptophan and its catabolites reduced chennluminescence according to a dose-response relationship, 3-hydroxvanthranilic acid being the most efficient compound. Apart from L-kynurenme the scavenging effects of tryptophan and its metabolites were not affected by changes m pH from 5.5 to 7.5. Our data indicate that tryptophan degradation produces metabolites with a high scavenging ability for reactive oxygen and chlorine species, thereby establishing a self-regulatory mechanism to limit the tissue damage by reactive radicals produced by macrophages.

scholarly journals Mildly Oxidized LDL Induces Expression of Group IIa Secretory Phospholipase A 2 in Human Monocyte–Derived Macrophages

2000 ◽  
Vol 20 (5) ◽  
pp. 1276-1282 ◽  
Author(s):  
Marit W. Anthonsen ◽  
Dominique Stengel ◽  
Delphine Hourton ◽  
Ewa Ninio ◽  
Berit Johansen
Keyword(s):  
Oxidized Ldl ◽  
Human Monocyte ◽  
Phospholipase A ◽  
Secretory Phospholipase ◽  
Phospholipase A 2
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