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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2001-11-13
pubmed:abstractText
Activation of the TNF signal transduction cascade is initiated by the interaction of TNF with either of two cell surface receptors, TNFR-1 and TNFR-2. The levels and regulation of expression of these two receptors has been extensively analyzed in cultured cells, but little is known of TNFR expression in situ. We analyzed the expression of TNFR-1 and -2 in normal human renal kidney and in renal transplants undergoing acute cellular rejection. Immunohistochemistry and immunogold electron microscopy indicated a strong expression of TNFR-1 on the endothelium of glomeruli of normal kidney. Immunogold colocalization for TNFR-1 and a marker of the trans-Golgi network (TGN-46) demonstrated TNFR-1 within the Golgi complex in endothelial cells in normal kidney, confirming our previous studies with cultured cells. TNFR-1 expression was lost in glomeruli from acutely rejecting kidney, but TNFR-1 was detected in abundance on infiltrating leukocytes in the interstitium of allografts with acute rejection. In contrast, TNFR-2 was demonstrated predominantly in epithelial cells of distal convoluted tubule (DCT) in acute rejection kidney near TNF-expressing leukocytes. TNF was absent in normal kidney, but present in rejecting allograft. TNF was found in infiltrating leukocytes and in adjacent tubular epithelial cells. In situ hybridization showed TNFR-1 mRNA within the endothelium of the glomeruli and of a few arterioles in normal kidney, whereas TNFR-2 mRNA was seen in tubular epithelial cells of the DCT in acute transplant rejection. These data reveal that there is both differential expression and regulation of the two TNF receptors in human kidney.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0023-6837
pubmed:author
pubmed:issnType
Print
pubmed:volume
81
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1503-15
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11706058-Acute Disease, pubmed-meshheading:11706058-Antigens, CD, pubmed-meshheading:11706058-Coloring Agents, pubmed-meshheading:11706058-Eosine Yellowish-(YS), pubmed-meshheading:11706058-Fluorescent Dyes, pubmed-meshheading:11706058-Gene Expression, pubmed-meshheading:11706058-Graft Rejection, pubmed-meshheading:11706058-Hematoxylin, pubmed-meshheading:11706058-Humans, pubmed-meshheading:11706058-Kidney, pubmed-meshheading:11706058-Kidney Failure, Chronic, pubmed-meshheading:11706058-Kidney Transplantation, pubmed-meshheading:11706058-Microscopy, Immunoelectron, pubmed-meshheading:11706058-Receptors, Tumor Necrosis Factor, pubmed-meshheading:11706058-Receptors, Tumor Necrosis Factor, Type I, pubmed-meshheading:11706058-Receptors, Tumor Necrosis Factor, Type II, pubmed-meshheading:11706058-Tumor Necrosis Factor-alpha
pubmed:year
2001
pubmed:articleTitle
Expression of tumor necrosis factor receptors in normal kidney and rejecting renal transplants.
pubmed:affiliation
Department of Medicine, University of Cambridge, Addenbrooke's Hospital, Cambridge, United Kingdom. rsma2@hermes.cam.ac.uk
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't