Evidence map›Paper›PMID 7657807›Full record

ArticleThe Journal of clinical investigation1995

AIDS-associated Kaposi's sarcoma (KS) cells express oncostatin M (OM)-specific receptor but not leukemia inhibitory factor/OM receptor or interleukin-6 receptor. Complete block of OM-induced KS cell growth and OM binding by anti-gp130 antibodies.

K Murakami-Mori, T Taga, T Kishimoto, S Nakamura

Abstract readComparative Study
In one paragraph

Article in The Journal of clinical investigation, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

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10citing papers in PubMed
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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

10 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

K Murakami-MoriInstitute of Molecular Medicine and Technology, Huntington Memorial Hospital, Pasadena, California 91105, USA.
T Taga
T Kishimoto
S Nakamura

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oncostatin M (OM), which shares functional similarity and structural homology to leukemia inhibitory factor (LIF) and interleukin-6 (IL-6), functions as a potent growth factor for AIDS-associated Kaposi's sarcoma-derived cells (AIDS-KS cells). OM was also suggested to bind to the LIF receptor (LIF/OM receptor), which consists of a signal transducing subunit for LIF and IL-6 (gp130) and a LIF receptor alpha-subunit. Recent studies indicate that IL-6 has growth-stimulating activity for AIDS-KS cells. However, we find that AIDS-KS cell growth is exclusively induced by OM and not by LIF or IL-6. We also observed the lack of binding properties of AIDS-KS cells for LIF and IL-6. Scatchard plots revealed the existence of two affinity classes of OM receptor sites on AIDS-KS cells, with Kd values of 6-12 pM (high affinity) and 521-815 pM (low affinity). In competition binding studies, we find that the OM-specific receptor, but not the LIF/OM receptor, contributes to the OM-specific growth stimulation of AIDS-KS cells. We also noted that anti-gp130 antibodies can completely abolish OM-induced growth stimulation of AIDS-KS cells as well as OM binding to AIDS-KS cells. PCR amplification clearly revealed high levels of gp130 expression in AIDS-KS cells, while the transcript of LIF receptor alpha-subunit or IL-6 receptor alpha-subunit was not observed. Therefore, we conclude that (a) AIDS-KS cells express the OM-specific receptor with high and low affinity, but not the LIF/OM receptor; (b) gp130 on AIDS-KS cells plays a key role in OM binding and signaling on the OM-specific receptor; and (c) the lack of biological response of AIDS-KS cells to IL-6 and LIF can be explained by the absence of the IL-6 and LIF/OM receptors. All this evidence shows the correlation of OM-specific biological activity with expression of the OM-specific receptor and the involvement of gp130 on this receptor, as based on findings in in vitro growth assays and binding experiments for AIDS-KS cells.

Indexed as

Gene ExpressionInterleukin-6Peptide BiosynthesisAcquired Immunodeficiency SyndromeAntibodies, MonoclonalBase SequenceCell DivisionCell LineDNA PrimersGrowth InhibitorsHumansKineticsLeukemia Inhibitory FactorLeukemia Inhibitory Factor Receptor alpha SubunitLymphokinesMolecular Sequence DataAntibodies, MonoclonalDNA PrimersGrowth InhibitorsInterleukin-6Leukemia Inhibitory FactorLeukemia Inhibitory Factor Receptor alpha SubunitLIF protein, humanLIFR protein, humanLymphokinesOncostatin MOSM protein, humanPeptidesReceptors, CytokineReceptors, InterleukinReceptors, Interleukin-6Receptors, Oncostatin MReceptors, OSM-LIF

Identifiers

PMID7657807
PMCPMC185754

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