scholarly journals Effects of Cigarette Smoke and Opium on the Expression of CD9, CD36, and CD68 at mRNA and Protein Levels in Human Macrophage Cell Line THP-1

2020 ◽  
Author(s):  
Mohammad Amin Momeni-Moghaddam ◽  
Gholamreza Asadikaram ◽  
Mohammad Hadi Nematollahi ◽  
Mojdeh Esmaeili Tarzi ◽  
Sanaz Faramarz-Gaznagh ◽  
...  
Keyword(s):  
Protein Expression ◽  
Cell Line ◽  
Cigarette Smoke ◽  
Cigarette Smoke Extract ◽  
Scavenger Receptors ◽  
Human Macrophage ◽  
Macrophage Cell Line ◽  
Macrophage Cell ◽  
Expression Levels ◽  
Protein Levels

Cigarette smoking and opium use are risk factors for coronary artery disease (CAD). It has been known that scavenger receptors such as CD36 and CD68 play critical roles in the pathogenesis of CAD. CD9, as a member of the tetraspanin, has been shown to interact with scavenger receptors. The aim of this study was to investigate the effects of these risk factors on expression levels of CD9, CD36, and CD68 on the THP-1 cell line. The THP-1 cell line treated with cigarette smoke extract (CSE( and opium, both individually and combinatory, in 24 h incubation. The protein and mRNA levels of CD9, CD36, and CD68 were evaluated by flow cytometry and quantitative reverse transcription-Polymerase Chain Reaction (qRT-PCR) techniques, respectively. CD36 and CD68 mRNA and protein expression levels were significantly increased in the cells treated with cigarette smoke extract compared to the control (p<0.001 in mRNA expression levels and p=0.016 and p=0.012 in protein expression levels, respectively). The CSE increased the level of CD9 protein expression compared to the control group (p=0.041) on the human macrophage cell line THP-1. No significant differences were observed in the CD9, CD36, and CD68 gene expression and at the protein levels between opium-treated THP-1 cells and controls. In conclusion, cigarettes by increasing the levels of CD36, CD68, and CD9 can be a risk factor in the development of many inflammatory diseases, including cardiovascular diseases, chronic obstructive pulmonary disease (COPD) and lung carcinoma.

Modulation of Fcγ receptors on the human macrophage cell line U-937

1989 ◽  
Vol 120 (1) ◽  
pp. 174-187 ◽  
Author(s):  
Milton D. Rossman ◽  
Edgar Chen ◽  
Paul Chien ◽  
Alan D. Schreiber
Keyword(s):  
Cell Line ◽  
Human Macrophage ◽  
Macrophage Cell Line ◽  
Macrophage Cell ◽  
Fcγ Receptors

scholarly journals Characterisation of a New Human Alveolar Macrophage-Like Cell Line (Daisy)

Lung ◽  
2019 ◽  
Vol 197 (6) ◽  
pp. 687-698
Author(s):  
Laura R. Sadofsky ◽  
Yvette A. Hayman ◽  
Jesse Vance ◽  
Jorge L. Cervantes ◽  
Simon D. Fraser ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Cell Line ◽  
Ex Vivo ◽  
Human Macrophage ◽  
Macrophage Cell Line ◽  
Binding Assays ◽  
Macrophage Cell ◽  
Mitogenic Stimulation ◽  
Human Alveolar Macrophage

Abstract Purpose There is currently no true macrophage cell line and in vitro experiments requiring these cells currently require mitogenic stimulation of a macrophage precursor cell line (THP-1) or ex vivo maturation of circulating primary monocytes. In this study, we characterise a human macrophage cell line, derived from THP-1 cells, and compare its phenotype to the THP-1 cells. Methods THP-1 cells with and without mitogenic stimulation were compared to the newly derived macrophage-like cell line (Daisy) using microscopy, flow cytometry, phagocytosis assays, antigen binding assays and gene microarrays. Results We show that the cell line grows predominantly in an adherent monolayer. A panel of antibodies were chosen to investigate the cell surface phenotype of these cells using flow cytometry. Daisy cells expressed more CD11c, CD80, CD163, CD169 and CD206, but less CD14 and CD11b compared with mitogen-stimulated THP-1 cells. Unlike stimulated THP-1 cells which were barely able to bind immune complexes, Daisy cells showed large amounts of immune complex binding. Finally, although not statistically significant, the phagocytic ability of Daisy cells was greater than mitogen-stimulated THP-1 cells, suggesting that the cell line is more similar to mature macrophages. Conclusions The observed phenotype suggests that Daisy cells are a good model of human macrophages with a phenotype similar to human alveolar macrophages.

Reduction of Sb(V) in a Human Macrophage Cell Line Measured by HPLC-ICP-MS

2011 ◽  
Vol 144 (1-3) ◽  
pp. 234-243 ◽  
Author(s):  
Claus Hansen ◽  
Erik Wind Hansen ◽  
Helle Rüsz Hansen ◽  
Bente Gammelgaard ◽  
Stefan Stürup
Keyword(s):  
Cell Line ◽  
Human Macrophage ◽  
Macrophage Cell Line ◽  
Macrophage Cell ◽  
Icp Ms

scholarly journals Elucidation of the Mechanism Underlying the Anti-Inflammatory Properties of (S)-(+)-Carvone Identifies a Novel Class of Sirtuin-1 Activators in a Murine Macrophage Cell Line

Biomedicines ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 777
Author(s):  
Cátia Sousa ◽  
Bruno Miguel Neves ◽  
Alcino Jorge Leitão ◽  
Alexandrina Ferreira Mendes
Keyword(s):  
Cell Line ◽  
Sirtuin 1 ◽  
Low Grade ◽  
Murine Macrophage ◽  
Macrophage Cell Line ◽  
Macrophage Cell ◽  
Murine Macrophage Cell Line ◽  
Protein Levels ◽  
Age Related ◽  
Anti Inflammatory

The signaling pathways involved in age-related inflammation are increasingly recognized as targets for the development of preventive and therapeutic strategies. Our previous study elucidated the structure–activity relationship of monoterpene compounds derived from p-menthane as potential anti-inflammatory drugs and identified (S)-(+)-carvone as the most potent among the compounds tested. This study aims at identifying the molecular mechanism underlying the anti-inflammatory properties of (S)-(+)-carvone. The murine macrophage cell line, Raw 264.7, was stimulated with bacterial lipopolysaccharide (LPS) to simulate inflammation. Western blot was used to assess protein levels and post-translational modifications. The subcellular localization of NF-κB/p65 was visualized by immunocytochemistry. An in vitro fluorometric assay was used to measure Sirtuin-1 (SIRT1) activity. (S)-(+)-carvone inhibited LPS-induced JNK1 phosphorylation, but not that of p38 and ERK1/2 and also did not affect the phosphorylation and degradation of the NF-κB inhibitor, IκB-α. Accordingly, (S)-(+)-carvone did not affect LPS-induced phosphorylation of NF-κB/p65 on Ser536 and its nuclear translocation, but it significantly decreased LPS-induced IκB-α resynthesis, a NF-κB-dependent process, and NF-κB/p65 acetylation on lysine (Lys) 310. Deacetylation of that Lys residue is dependent on the activity of SIRT1, which was found to be increased by (S)-(+)-carvone, while its protein levels were unaffected. Taken together, these results show that (S)-(+)-carvone is a new SIRT1 activator with the potential to counteract the chronic low-grade inflammation characteristic of age-related diseases.

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