Role of Interleukins and Nitric Oxide Secretion by Peritoneal Macrophages in Differential Tumoricidal Effect to Transplantable Melanomas as Regarding their Biological Properties

Kozłowska, K; Cichorek, M; Wachulska, Małgorzata; Bautembach, I.

doi:10.1080/08923970600809413

Cited by 6 publications

(1 citation statement)

References 25 publications

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“…Upon activation, macrophages produce many types of inflammatory mediators, such as interleukin (IL)-6, tumor necrosis factor (TNF)-α, and nitric oxide (NO) molecules that are central to the immunoregulatory function of macrophages (12)(13)(14). The NO produced by inducible NOS (iNOS) is a major acute and chronic inflammatory mediator (15,16).…”

Section: Activation Of Raw2647 Mouse Macrophage Cells In Vitro Throumentioning

confidence: 99%

Activation of RAW264.7 mouse macrophage cells in vitro through treatment with recombinant ricin toxin-binding subunit B: Involvement of protein tyrosine, NF-κB and JAK-STAT kinase signaling pathways

Yuan

Liu

et al. 2013

International Journal of Molecular Medicine

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Ricin toxin-binding subunit B (RTB) is a galactose-binding lectin protein. In the present study, we investigated the effects of RTB on inducible nitric oxide (NO) synthase (iNOS), interleukin (IL)-6 and tumor necrosis factor (TNF)-α, as well as the signal transduction mechanisms involved in recombinant RTB-induced macrophage activation. RAW264.7 macrophages were treated with RTB. The results revealed that the mRNA and protein expression of iNOS was increased in the recombinant RTB-treated macrophages. TNF-α production was observed to peak at 20 h, whereas the production of IL-6 peaked at 24 h. In another set of cultures, the cells were co-incubated with RTB and the tyrosine kinase inhibitor, genistein, the phosphatidylinositol 3-kinase (PI3K) inhibitor, LY294002, the p42/44 inhibitor, PD98059, the p38 inhibitor, SB203580, the JNK inhibitor, SP600125, the protein kinase C (PKC) inhibitor, staurosporine, the JAK2 inhibitor, tyrphostin (AG490), or the NOS inhibitor, L-NMMA. The recombinant RTB-induced production of NO, TNF-α and IL-6 was inhibited in the macrophages treated with the pharmacological inhibitors genistein, LY294002, staurosporine, AG490, SB203580 and BAY 11-7082, indicating the possible involvement of protein tyrosine kinases, PI3K, PKC, JAK2, p38 mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-κB in the above processes. A phosphoprotein analysis identified tyrosine phosphorylation targets that were uniquely induced by recombinant RTB and inhibited following treatment with genistein; some of these proteins are associated with the downstream cascades of activated JAK-STAT and NF-κB receptors. Our data may help to identify the most important target molecules for the development of novel drug therapies.

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Section: Activation Of Raw2647 Mouse Macrophage Cells In Vitro Throumentioning

confidence: 99%

Activation of RAW264.7 mouse macrophage cells in vitro through treatment with recombinant ricin toxin-binding subunit B: Involvement of protein tyrosine, NF-κB and JAK-STAT kinase signaling pathways

Yuan

Liu

et al. 2013

International Journal of Molecular Medicine

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Hybrids of carbon dots with subunit B of ricin toxin for enhanced immunomodulatory activity

Liu

Sun

et al. 2018

Journal of Colloid and Interface Science

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Production of nitric oxide by murine peritoneal macrophages in vitro on treatment with prolactin and growth hormone: Involvement of protein tyrosine kinases, Ca++, and MAP kinase signal transduction pathways

Tripathi

Sodhi

2007

Molecular Immunology

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Role of Interleukins and Nitric Oxide Secretion by Peritoneal Macrophages in Differential Tumoricidal Effect to Transplantable Melanomas as Regarding their Biological Properties

Cited by 6 publications

References 25 publications

Activation of RAW264.7 mouse macrophage cells in vitro through treatment with recombinant ricin toxin-binding subunit B: Involvement of protein tyrosine, NF-κB and JAK-STAT kinase signaling pathways

Activation of RAW264.7 mouse macrophage cells in vitro through treatment with recombinant ricin toxin-binding subunit B: Involvement of protein tyrosine, NF-κB and JAK-STAT kinase signaling pathways

Hybrids of carbon dots with subunit B of ricin toxin for enhanced immunomodulatory activity

Production of nitric oxide by murine peritoneal macrophages in vitro on treatment with prolactin and growth hormone: Involvement of protein tyrosine kinases, Ca++, and MAP kinase signal transduction pathways

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