Source:http://linkedlifedata.com/resource/pubmed/id/12700958
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2003-4-17
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pubmed:abstractText |
Macrophages play important roles during renal inflammation. Infiltrating macrophages produce proinflammatory mediators and induce apoptosis in a variety of target cells. Because proximal tubules are frequently damaged in inflammatory processes, we investigated murine macrophages (J774) in the induction of apoptosis in murine PKSV-PR proximal tubule cells. PKSV-PR cells were co-cultured with activated or non-activated macrophages. Apoptosis was assessed by Annexin-V-FITC/propidium iodide staining and analyzed by fluorescence-activated cell sorting. Macrophages were separated from tubule cells with transwell membranes to distinguish soluble factor-mediated from direct cell-to-cell contact-mediated apoptosis. Cell supernatants from activated and non-activated macrophages were analyzed for induction of apoptosis. Activated (but not non-activated) macrophages induced tubule cell apoptosis in co-culture. Soluble factors were mainly responsible for induction of apoptosis; membrane separation and transfer of cell supernatant from activated macrophages showed similar levels of apoptosis induction. Although tumor necrosis factor (TNF)-alpha and transforming growth factor (TGF)-beta(1), measured by ELISA, increased significantly in supernatants from activated macrophages, blocking TNF-alpha and TGF-beta did not decrease apoptosis in PKSV-PR cells co-cultured with macrophages. Moreover, exogenous addition of TNF-alpha, TGF-beta, anti-Fas antibody, or TRAIL failed to induce apoptosis in tubule cells. We conclude that inflammatory macrophages mediate proximal tubule cell death, directing apoptosis mainly via release of unidentified soluble factors.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD95,
http://linkedlifedata.com/resource/pubmed/chemical/Apoptosis Regulatory Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Culture Media, Conditioned,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/TNF-Related Apoptosis-Inducing...,
http://linkedlifedata.com/resource/pubmed/chemical/Tnfsf10 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0931-041X
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
18
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
335-41
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:12700958-Animals,
pubmed-meshheading:12700958-Antigens, CD95,
pubmed-meshheading:12700958-Apoptosis,
pubmed-meshheading:12700958-Apoptosis Regulatory Proteins,
pubmed-meshheading:12700958-Cell Line,
pubmed-meshheading:12700958-Coculture Techniques,
pubmed-meshheading:12700958-Culture Media, Conditioned,
pubmed-meshheading:12700958-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:12700958-Flow Cytometry,
pubmed-meshheading:12700958-Kidney Tubules, Proximal,
pubmed-meshheading:12700958-Macrophage Activation,
pubmed-meshheading:12700958-Macrophages,
pubmed-meshheading:12700958-Membrane Glycoproteins,
pubmed-meshheading:12700958-Mice,
pubmed-meshheading:12700958-Subcellular Fractions,
pubmed-meshheading:12700958-TNF-Related Apoptosis-Inducing Ligand,
pubmed-meshheading:12700958-Transforming Growth Factor beta,
pubmed-meshheading:12700958-Tumor Necrosis Factor-alpha
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pubmed:year |
2003
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pubmed:articleTitle |
Macrophages induce apoptosis in proximal tubule cells.
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pubmed:affiliation |
Department of Pediatrics, University of Virginia, VA 22908, Charlottesville, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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