Oncostatin M as a Potent Mitogen for AIDS-Kaposi's Sarcoma-Derived Cells

Miles, Steven A.; Martı́nez-Maza, Otoniel; Rezai, Ahmad; Magpantay, Larry; Kishimoto, T; Nakamura, Shuji; Radka, Susan F.; Linsley, Peter S.

doi:10.1126/science.1542793

Cited by 234 publications

(81 citation statements)

References 14 publications

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“…As a consequence, some biological effects are shared by OSM and LIF, whereas others are OSM-specific. OSM is known to be a growth regulator which stimulates the growth of fibroblasts (18), vascular smooth muscle cells (19), and Kaposi's sarcoma cells (20).…”

Section: Oncostatin M Stimulates the Growth Of Dermal Fibroblastsmentioning

confidence: 99%

Oncostatin M Stimulates the Growth of Dermal Fibroblasts Via a Mitogen-Activated Protein Kinase-Dependent Pathway

Ihn

Tamaki

2000

The Journal of Immunology

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Oncostatin M (OSM), a member of the hemopoietic cytokine family, has been implicated in the process of fibrosis and dermal wound healing. As a part of an ongoing study of the mechanisms of fibrosis and dermal wound healing, we have investigated the mechanism of the growth regulation of dermal fibroblasts by OSM. OSM stimulates the mitogenesis of dermal fibroblasts in a dose-dependent manner. This effect was completely blocked by anti-OSM IgG, but not by anti-IL-6 IgG. Furthermore, OSM induction was abolished by genistein, a tyrosine kinase inhibitor, or by PD98059, a specific mitogen-activated protein (MAP) kinase pathway inhibitor, but not by calphostin C, a protein kinase C inhibitor. Immunoblotting analysis using a specific Ab against phosphorylated MAP kinase (Thr202/Tyr204) showed that OSM induces phosphorylation of MAP kinase in dermal fibroblasts. Furthermore, transient transfection of the dominant-negative mutant MAP kinase into dermal fibroblasts abolished the OSM induction. These results strongly suggest that OSM stimulates the growth of dermal fibroblasts via a MAP kinase-dependent pathway.

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Section: Oncostatin M Stimulates the Growth Of Dermal Fibroblastsmentioning

confidence: 99%

Oncostatin M Stimulates the Growth of Dermal Fibroblasts Via a Mitogen-Activated Protein Kinase-Dependent Pathway

Ihn

Tamaki

2000

The Journal of Immunology

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“…Second, endothelial cells respond to oncostatin M with activation of MAP kinase activity (11), IL-6 secretion (9), and delayed, but prolonged, P-selectin synthesis (12). Third, oncostatin M is the major autocrine growth factor for Kaposi's sarcoma cells (13), and these spindle-shaped cells are thought to be of endothelial cell origin (14,15).…”

Section: Introductionmentioning

confidence: 99%

Oncostatin M is a proinflammatory mediator. In vivo effects correlate with endothelial cell expression of inflammatory cytokines and adhesion molecules.

Modur¹,

Feldhaus²,

Weyrich³

et al. 1997

J. Clin. Invest.

181

139

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“…6,7 Of particular interest are the findings that these cells secrete and respond to interleukin-6 (IL-6) and oncostatin M (OSM) suggesting a possible autocrine and/or paracrine growth regulation. 6,[8][9][10] HHV-8 infection may conceivably cause the cytokine production in these cells. 11 It is known that viral genes can transactivate cellular genes; such transactivation is thought to be one of the mechanisms of tumorigenesis.…”

Section: Introductionmentioning

confidence: 99%

Constitutive cytokine production by primary effusion (body cavity-based) lymphoma-derived cell lines

et al. 1999

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. In addition, we tested the response of the PEL cells to selected cytokines and the effects of neutralizing anti-cytokine and anti-cytokine receptor antibodies. Using specific ELISAs, PEL cell lines were found to produce large amounts of interleukin-6 (IL-6; 10-5000 pg/ml), IL-6 soluble receptor (IL-6sR; 30-600 pg/ml), IL-10 (600-80 000 pg/ml) and oncostatin M (OSM; 50-80 pg/ml) which in most cases were significantly higher than the levels produced by the Burkitt, B-NHL or myeloma cell lines; on the contrary, PEL cell lines did not elaborate significant levels of macrophage inhibitory protein (MIP-1␣) and leukemia inhibitory factor (LIF). However, the levels of MIP-1␣ were increased 10-to 100-fold by treatment with phorbol ester TPA. PEL cell lines did not respond proliferatively to IL-6, IL-10, IL-11, LIF, MIP-1␣, or OSM. Incubation with IL-6sR and IL-6 inhibited cell growth. Anti-IL6 neutralizing antibodies had no effect on PEL cell line proliferation; conversely, whereas anti-IL6R alone inhibited only weakly, anti-gp130 and anti-gp130 plus anti-IL6R showed strong inhibitory effects (Ͼ20% inhibition in 5/9 lines and Ͼ60% inhibition in 3/9 lines). In summary, PEL cell lines produce high amounts of cytokines (IL-6, IL-10, OSM); proliferation could be inhibited by blocking the receptors of the IL-6 signaling pathway.

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Oncostatin M as a Potent Mitogen for AIDS-Kaposi's Sarcoma-Derived Cells

Cited by 234 publications

References 14 publications

Oncostatin M Stimulates the Growth of Dermal Fibroblasts Via a Mitogen-Activated Protein Kinase-Dependent Pathway

Oncostatin M Stimulates the Growth of Dermal Fibroblasts Via a Mitogen-Activated Protein Kinase-Dependent Pathway

Oncostatin M is a proinflammatory mediator. In vivo effects correlate with endothelial cell expression of inflammatory cytokines and adhesion molecules.

Constitutive cytokine production by primary effusion (body cavity-based) lymphoma-derived cell lines

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