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rdf:type |
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lifeskim:mentions |
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pubmed:dateCreated |
2010-3-18
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pubmed:abstractText |
We have recently shown that oxidative stress of ARPE-19 cells alters the expression of the cell surface complement regulatory proteins DAF and CD59, and permits increased activation of complement when the cells are subsequently exposed to serum. Based upon these results, we hypothesized that RPE cells respond to cellular stress as if it is infection, and reduce their surface expression of complement regulatory proteins to foster the local immune response. To test this hypothesis, we examined whether cellular hypoxia would produce a similar change in ARPE-19 cells. In addition, we asked whether this response to oxidative stress is universal in all epithelial cells, by examining the expression of complement regulatory proteins on the surface of the renal and pulmonary epithelial cells. We found that the expression of complement regulatory proteins is altered by aseptic cellular stressors such as hypoxia and oxidative stress, but the response to these conditions differs from tissue to tissue. In RPE cells oxidative stress reduces the expression of the cell surface complement regulators and sensitizes the cells to complement mediated injury. This specific response is not seen in epithelial cells from the lung or kidney, and is not induced by hypoxia. These studies help explain the unique mechanisms by which uncontrolled complement activation may contribute to the development of AMD.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD46,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD55,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD59,
http://linkedlifedata.com/resource/pubmed/chemical/CD46 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Complement System Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Crry protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Complement
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pubmed:status |
MEDLINE
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pubmed:issn |
0065-2598
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
664
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
151-8
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pubmed:meshHeading |
pubmed-meshheading:20238013-Animals,
pubmed-meshheading:20238013-Antigens, CD46,
pubmed-meshheading:20238013-Antigens, CD55,
pubmed-meshheading:20238013-Antigens, CD59,
pubmed-meshheading:20238013-Cell Hypoxia,
pubmed-meshheading:20238013-Cell Line,
pubmed-meshheading:20238013-Cell Membrane,
pubmed-meshheading:20238013-Complement Activation,
pubmed-meshheading:20238013-Complement System Proteins,
pubmed-meshheading:20238013-Epithelial Cells,
pubmed-meshheading:20238013-Flow Cytometry,
pubmed-meshheading:20238013-Humans,
pubmed-meshheading:20238013-Kidney Tubules,
pubmed-meshheading:20238013-Lung,
pubmed-meshheading:20238013-Mice,
pubmed-meshheading:20238013-Organ Specificity,
pubmed-meshheading:20238013-Oxidative Stress,
pubmed-meshheading:20238013-Receptors, Complement
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pubmed:year |
2010
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pubmed:articleTitle |
Aseptic injury to epithelial cells alters cell surface complement regulation in a tissue specific fashion.
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pubmed:affiliation |
Department of Medicine, University of Colorado Denver School of Medicine, Denver, CO 80045, USA.
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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