Signal transduction of phorbol 12-myristate 13-acetate (PMA)-induced growth inhibition of human monocytic leukemia THP-1 cells is reactive oxygen dependent

Traore, Kassim; Trush, Michael A.; George, Matthew; Spannhake, E. W.; Anderson, Winston A.; Asseffa, Amha

doi:10.1016/j.leukres.2004.12.011

Cited by 105 publications

(111 citation statements)

References 56 publications

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“…3B). Moreover, similar alteration in the expression of AKR1C1, AKR1C3 and NQO1 was observed when the cells were incubated with phorbol 12-myristate 13-acetate (PMA), an inducer of differentiation via the enhanced ROS generation 32) (Fig. 3A(b)).…”

Section: )supporting

confidence: 57%

9,10-Phenanthrenequinone Induces Monocytic Differentiation of U937 Cells through Regulating Expression of Aldo-Keto Reductase 1C3

Matsunaga

Hosogai

Arakaki

et al. 2012

Biological & Pharmaceutical Bulletin

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Persistent inhalation of diesel exhaust particles results in damaged lung cells through formation of reactive oxygen species (ROS), but the details of the toxicity mechanism against monocytes are poorly understood. In this study, we used human promyelomonocytic U937 cells as surrogates of monocytes and investigated the toxicity mechanism initiated by exposure to 9,10-phenanthrenequinone (9,10-PQ), a major quinone component in diesel exhaust particles. A 24-h incubation with 9,10-PQ provoked apoptotic cell death, which was due to signaling through the enhanced ROS generation and concomitant caspase activation. Flow cytometric analyses of U937 cells after long-term exposure to 9,10-PQ revealed induction of differentiation that was evidenced by increasing expression of CD11b/CD18, a cell-surface marker for monocytic differentiation into macrophages. The 9,10-PQ-induced differentiation was significantly abolished by ROS inhibitors, suggesting that ROS generation contributes to cell differentiation. The 9,10-PQ treatment increased the expression of aldo-keto reductase (AKR) 1C3, which reached a peak at 1 to 2 d post-treatment and then declined. The bell-shaped curve of the AKR1C3 expression by 9,10-PQ resembled that caused by phorbol 12-myristate 13-acetate, a differentiation inducer. Additionally, the concomitant treatment with tolfenamic acid, a selective AKR1C3 inhibitor, sensitized the differentiation induced by 9,10-PQ. These results suggest that ROS formation during 9,10-PQ treatment acutely leads to apoptosis of U937 cells and the initiation of monocytic differentiation, which proceeds after the provisional overexpression of AKR1C3.Key words 9,10-phenanthrenequinone; differentiation; aldo-keto reductase 1C3; U937; oxidative stress Diesel exhaust particles (DEP) are believed to be harmful air pollutants that cause significant impediments to respiratory function leading to asthma and carcinogenesis.1,2) The mechanisms underlying their disorders is very complicated due to the involvement of a variety of lung cells such as epithelial cells, macrophages and lymphocytes.2) In the acute phase, macrophages are directly activated in response to stimulation with DEP resulting in the regulation of the immune signaling networks through secretion of pro-inflammatory mediators, cytokines 3) and chemokines. 4) In addition, the inhalation of DEP was shown to increase the number of lung macrophages, 5) which may be involved in clearing the particles by phagocytotic ingestion. 6) Thus, macrophages are believed to play pivotal roles in the cytoprotective responses against DEP. On the other hand, several researchers found that the administration of DEP lowers both antimicrobial and mitochondrial functions in alveolar macrophages through generation of reactive oxygen species (ROS) in addition to activating apoptotic signaling. 7,8) DEP are heterogeneous species that consist of a variety of organic and inorganic chemicals, such as polycyclic aromatic hydrocarbons, nitroaromatic hydrocarbons, heterocycles, aldehydes and quinones. 9)...

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Section: )supporting

confidence: 57%

9,10-Phenanthrenequinone Induces Monocytic Differentiation of U937 Cells through Regulating Expression of Aldo-Keto Reductase 1C3

Matsunaga

Hosogai

Arakaki

et al. 2012

Biological & Pharmaceutical Bulletin

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“…For phagocytosis assay, THP-1 cells were cultured at an initial density of 1 ϫ 10 6 cells/well on six-well plates (Greiner, Frickenhausen, Germany) for 24 h and treated with phorbol 12-myristate 13-acetate at a final concentration of 100 nM for 24 h to facilitate differentiation into macrophages (51). After treatment, the adherent macrophages were washed three times with phosphate-buffered saline (PBS) and incubated with cell culture medium.…”

Section: Methodsmentioning

confidence: 99%

Surface Lipoprotein PpiA of Streptococcus mutans Suppresses Scavenger Receptor MARCO-Dependent Phagocytosis by Macrophages

et al. 2011

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Streptococcus mutans is associated with the initiation and progression of human dental caries and is occasionally isolated from the blood of patients with bacteremia and infective endocarditis. For the pathogen to survive in the infected host, surface lipoproteins of S. mutans are likely to play important roles in interactions with the innate immune system. To clarify the role that a putative lipoprotein, peptidyl-prolyl cis/transisomerase (PpiA), of S. mutans plays in the macrophage response, we investigated the response of THP-1-derived macrophages to S. mutans challenge. The deletion of the gene encoding Lgt eliminated PpiA on the cell surface of S. mutans, which implies that PpiA is a lipoprotein that is lipid anchored in the cell membrane by Lgt. Human and murine peritoneal macrophages both showed higher phagocytic activities for the ppiA and lgt mutants than the wild type, which indicates that the presence of PpiA reduces S. mutans phagocytosis. In addition, infection with S. mutans markedly induced mRNAs of macrophage receptor with collagenous structure (MARCO) and scavenger receptor A (SR-A) in human macrophages. In particular, transcriptional and translational levels of MARCO in human macrophages infected with the ppiA mutant were higher than those in macrophages infected with the wild type. Phagocytosis of S. mutans by human macrophages markedly decreased after treatment with anti-MARCO IgG. These results demonstrate that the S. mutans lipoprotein PpiA contributes to suppression of MARCO-mediated phagocytosis of this bacterium by macrophages.

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“…Others have reported that PKCdelta is upstream of changes in mitochondrial memebrane leading to cytochrome c release (Liao et al, 2005) and PKCzeta is upstream of p38 MAPK activation in UVB-induced apoptosis (Won et al, 2005). ROS may be upstream of PKC because it has been shown that PKC-dependent induction of p21WAF1 by phorbol ester was inhibited by antioxidant (Traore et al, 2005).…”

Section: Hpr-induced Apoptosis In Hnscc Cellsmentioning

confidence: 99%

N-(4-Hydroxyphenyl)retinamide-induced apoptosis triggered by reactive oxygen species is mediated by activation of MAPKs in head and neck squamous carcinoma cells

et al. 2006

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Signal transduction of phorbol 12-myristate 13-acetate (PMA)-induced growth inhibition of human monocytic leukemia THP-1 cells is reactive oxygen dependent

Cited by 105 publications

References 56 publications

9,10-Phenanthrenequinone Induces Monocytic Differentiation of U937 Cells through Regulating Expression of Aldo-Keto Reductase 1C3

9,10-Phenanthrenequinone Induces Monocytic Differentiation of U937 Cells through Regulating Expression of Aldo-Keto Reductase 1C3

Surface Lipoprotein PpiA of Streptococcus mutans Suppresses Scavenger Receptor MARCO-Dependent Phagocytosis by Macrophages

N-(4-Hydroxyphenyl)retinamide-induced apoptosis triggered by reactive oxygen species is mediated by activation of MAPKs in head and neck squamous carcinoma cells

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