Document Detail


Correlation of oncostatin M secretion by human retrovirus-infected cells with potent growth stimulation of cultured spindle cells from AIDS-Kaposi's sarcoma.
MedLine Citation:
PMID:  8098726     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Oncostatin M (OM), a 30-kDa glycoprotein, recently was identified as a major growth-promoting factor in the conditioned medium (CM) of the 38-0 cell line, a CD4,+ chronically human T lymphotropic virus type (HTLV)-II-infected, transformed T cell line. CM 38-0 induced the proliferation of spindle cells cultured in vitro from AIDS-associated Kaposi's sarcoma (AIDS-KS) cells. To determine how much of the AIDS-KS cell growth activity present in 38-0 CM was because of the presence of OM, we depleted OM by using specific mAb-affinity chromatography. OM purified from this CM stimulated AIDS-KS cell growth in a concentration-dependent fashion. The effluent, completely depleted of OM, failed to induce growth of AIDS-KS cells. To detect the constitutive release of OM by cells acutely or chronically infected with either HTLV-I, HTLV-II, or HIV-1, we utilized an enzyme-linked immunoassay. Whereas the chronically infected cells released significant levels of OM, the acutely infected cells released little or no OM. The presence of OM in HIV-1-infected T-cell CM correlated completely with AIDS-KS cell growth activity. Infrequently, low level AIDS-KS cell growth activity was seen in the absence of OM. This correlated with relatively high levels of IL-6 in the CM. In a CM-containing OM in the absence of detectable IL-6, a neutralizing antibody to OM completely abrogated KS cell growth activity. The presence of specific oncostatin M receptors on the KS cell lines was confirmed by cross-linking experiments. The results shown here suggest that T cells chronically infected with HIV-1 can secrete OM, which may play a role in the initiation or progression of AIDS-KS lesions, either alone, or in concert with IL-6.
Authors:
S F Radka; S Nakamura; S Sakurada; S Z Salahuddin
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  150     ISSN:  0022-1767     ISO Abbreviation:  J. Immunol.     Publication Date:  1993 Jun 
Date Detail:
Created Date:  1993-06-22     Completed Date:  1993-06-22     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  5195-201     Citation Subset:  AIM; IM; X    
Affiliation:
Bristol-Myers Squibb Pharmaceutical Research Institute, Seattle, WA 98121.
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MeSH Terms
Descriptor/Qualifier:
Acquired Immunodeficiency Syndrome / metabolism*,  pathology*
Antibodies, Monoclonal / pharmacology
Cell Division / drug effects
Cells, Cultured
Chromatography, Affinity
Cross-Linking Reagents
Culture Media, Conditioned
Deltaretrovirus Infections / metabolism*
Growth Substances / secretion*
HIV Infections / metabolism*
Humans
Interleukin-6 / analysis
Oncostatin M
Peptides / analysis,  immunology,  secretion*
Receptors, Cell Surface / chemistry
Sarcoma, Kaposi / metabolism*,  pathology
Chemical
Reg. No./Substance:
0/Antibodies, Monoclonal; 0/Cross-Linking Reagents; 0/Culture Media, Conditioned; 0/Growth Substances; 0/Interleukin-6; 0/OSM protein, human; 0/Peptides; 0/Receptors, Cell Surface; 106956-32-5/Oncostatin M

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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