Source:http://linkedlifedata.com/resource/pubmed/id/19323971
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
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| pubmed:dateCreated |
2009-4-13
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| pubmed:abstractText |
Although previous studies have demonstrated that microvascular dysfunction and inflammation occur in ischemia-reperfusion injury (IRI), the underlying mechanisms are poorly understood. We hypothesized that T cells could mediate renal vascular permeability (RVP) during IRI. We evaluated renal vascular permeability by extravasation of Evans blue dye from the kidney in CD3, CD4 or CD8 T cell deficient mice as well as in TNF receptor knock out mice in our mouse model of kidney ischemia-reperfusion injury. In wild type mice, RVP was significantly increased at 3 h, peaked at 6 h and declined by 24 h after ischemia. Immunohistochemistry revealed that CD3(+) T cells trafficked into ischemic kidney at 1 h and peaked at 6 h. Gene microarray analysis demonstrated that endothelial-related genes including TNF-alpha were up-regulated in ischemic kidney. The production of TNF-alpha and IFN-gamma protein was increased in CD3 and CD4 T cells from the blood and kidney after ischemia. The rise in RVP after ischemia in wild type mice was attenuated in CD3, CD4 or CD8 T cell deficient mice as well as in TNF receptor knock out mice. The attenuation of RVP in CD3 T-cell deficient mice after ischemia was restored by adoptive transfer of T cells from WT mice. Our data demonstrate that T cells directly contribute to the increased RVP after kidney ischemia-reperfusion, potentially through T cell cytokine production.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
May
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| pubmed:issn |
1095-9319
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:volume |
77
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
340-7
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| pubmed:meshHeading |
pubmed-meshheading:19323971-Adoptive Transfer,
pubmed-meshheading:19323971-Animals,
pubmed-meshheading:19323971-Capillary Permeability,
pubmed-meshheading:19323971-Disease Models, Animal,
pubmed-meshheading:19323971-Immunoenzyme Techniques,
pubmed-meshheading:19323971-Interferon-gamma,
pubmed-meshheading:19323971-Kidney,
pubmed-meshheading:19323971-Mice,
pubmed-meshheading:19323971-Mice, Inbred C57BL,
pubmed-meshheading:19323971-Mice, Knockout,
pubmed-meshheading:19323971-Mice, Nude,
pubmed-meshheading:19323971-Oligonucleotide Array Sequence Analysis,
pubmed-meshheading:19323971-Recovery of Function,
pubmed-meshheading:19323971-Reperfusion Injury,
pubmed-meshheading:19323971-T-Lymphocyte Subsets,
pubmed-meshheading:19323971-Tumor Necrosis Factor-alpha,
pubmed-meshheading:19323971-Up-Regulation
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| pubmed:year |
2009
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| pubmed:articleTitle |
Effect of T cells on vascular permeability in early ischemic acute kidney injury in mice.
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| pubmed:affiliation |
Division of Nephrology, Johns Hopkins University School of Medicine, 720 Rutland Ave., Baltimore, MD 21205, USA. manchang@jhmi.edu
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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