Activated peritoneal macrophages inhibit the proliferation of rat ascites hepatoma AH-130 cells via the production of tumor necrosis factor- α and nitric oxide

Maekawa, Hisato; Iwabuchi, Kazuhisa; Nagaoka, Isao; Watanabe, Hidenobu; Kamano, Toshiki; Takahashi, Masahīko

doi:10.1007/s000110050629

Cited by 11 publications

(4 citation statements)

References 29 publications

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“…Maekawa et al [24] recently demonstrated that peritoneal macrophages activated by LPS and IL-2 suppressed the proliferation of ascites hepatoma AH-130 cells via the production of TNF-alpha and NO. It has been shown that eNOS-overexpressing endothelial cells significantly inhibited smooth muscle cells proliferation in vitro [25].…”

Section: Discussionmentioning

confidence: 97%

Nitric oxide inhibits ghrelin-induced cell proliferation and ERK1/2 activation in GH3 cells

Tian

Wang

et al. 2010

Endocr

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Ghrelin stimulates growth hormone release and cell proliferation, which strongly supports a significant role for this peptide in the control of growth hormone-releasing adenomas function and growth. Nitric oxide can influence the stimulatory effects of ghrelin on growth hormone secretion in growth hormone-releasing adenomas. However, the effect of nitric oxide (NO) on ghrelin-induced cell proliferation and the mechanism of this effect in the adenoma were not clarified. In this study, we observed that ghrelin, at a concentration of 10⁻⁹ to 10⁻⁶ M, significantly increased BrdU incorporation into rat GH3 cells. A NO donor, S-nitroso-N-acetylpenicillamine (SNAP), blunted basal, and ghrelin-induced cell proliferation. A blocker of NO synthase, Nw-nitro-L-arginine methyl ester hydrochloride (NAME), had no influence on these actions. The activation of extracellular signal-regulated kinase (ERK) 1/2 was examined by western blotting. The results showed that SNAP reduced ghrelin-stimulated ERK1/2 activation but NAME had no influence on this activation. Together, this study indicates that NO inhibited ghrelin-induced cell proliferation by blocking ERK1/2 activation in GH3 cells.

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Section: Discussionmentioning

confidence: 97%

Nitric oxide inhibits ghrelin-induced cell proliferation and ERK1/2 activation in GH3 cells

Tian

Wang

et al. 2010

Endocr

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“…Macrophages produce cytokines such as TNF-a and IL-6 and free radicals such as superoxide and nitric oxide (NO) (Maekawa et al, 2000). As mentioned above, the jellyfish collagen stimulated the phagocytotic activity of J774.1 cells.…”

Section: Cells and P-macmentioning

confidence: 97%

Effect of collagens from jellyfish and bovine Achilles tendon on the activity of J774.1 and mouse peritoneal macrophage cells

Putra

Morishige

Nishimoto

et al. 2012

Journal of Functional Foods

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“…Moreover, tumor cells inhibit the production of reactive oxygen intermediates by macrophages [22]. A rather inconsistent pattern emerges from the studies on the influence of tumor cells on NO release by the monocyte-macrophage lineage; stimulatory in the case of leukaemia, lymphoma, mastocytoma [23][24][25], ascites hepatoma [26], fibrosarcoma [27], and colon carcinoma cells [28,29]; inhibitory in the case of mammary carcinoma [30,31] and murine melanoma [32].…”

Section: Introductionmentioning

confidence: 98%

Enhancement of Nitric Oxide Release in Mouse Inflammatory Macrophages Co-cultivated with Tumor Cells of a Different Origin

Calorini

Bianchini

Mannini

et al. 2005

Clin Exp Metastasis

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In the present study we investigated whether synthesis of nitric oxide (NO) by macrophages is affected by contact with tumor cells. Although it is well known that NO generated by macrophages influences different activities related to tumor progression, there is limited information on the modulatory role of tumor cells on NO release by macrophages. The experimental protocol used in our study consisted in the determination of NO secreted by macrophages, either resident or inflammatory, co-cultivated with tumor cells (B16 melanoma and L929 fibrosarcoma cells) at different cell densities and macrophage:tumor cell ratios. This experimental in vitro protocol simulates the different interactions between macrophages and tumor cells that occur during the development of a tumor mass. We found that the co-cultivation with tumor cells induced an increased secretion of NO in macrophages provided that they express an inflammatory phenotype, and they were challenged with LPS or IFNgamma/LPS. Two more variables were found to be critical in the increase of NO generation in inflammatory macrophages cultivated with tumor cells: a high cell density and a prevalence of tumor cells over macrophages. The enhancement of NO secreted in inflammatory macrophages stimulated by tumor cells was not observed in normal murine fibroblasts co-cultivated with tumor cells.

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Activated peritoneal macrophages inhibit the proliferation of rat ascites hepatoma AH-130 cells via the production of tumor necrosis factor- α and nitric oxide

Abstract: Together these observations suggest that when peritoneal macrophages are activated by LPS and IL-2, they suppress the proliferation of ascites hepatoma AH-130 cells via the production of TNF-alpha and nitric oxide.

Cited by 11 publications

References 29 publications

Nitric oxide inhibits ghrelin-induced cell proliferation and ERK1/2 activation in GH3 cells

Nitric oxide inhibits ghrelin-induced cell proliferation and ERK1/2 activation in GH3 cells

Effect of collagens from jellyfish and bovine Achilles tendon on the activity of J774.1 and mouse peritoneal macrophage cells

Enhancement of Nitric Oxide Release in Mouse Inflammatory Macrophages Co-cultivated with Tumor Cells of a Different Origin

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