Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2006-6-9
pubmed:abstractText
HIV-associated nephropathy (HIVAN) is the most common cause of chronic renal failure in HIV-infected patients. Tubulointerstitial inflammation is a prominent component of the histopathology of HIVAN. The pathogenesis of HIVAN is a result of infection of renal epithelial cells, but the cellular response to this infection remains poorly defined. In these studies, we used oligonucleotide microarrays to identify differentially expressed genes in renal tubular epithelial cells from a patient with HIVAN at three time points after infection with vesicular stomatitis virus-pseudotyped gag/pol-deleted HIV-1. Very few genes were differentially expressed 12 and 24 hours after infection. Three days after infection, however, 47 genes were upregulated by at least 1.8-fold. The most prominent response of these cells to HIV-1 expression was production of proinflammatory mediators, including chemokines, cytokines, and adhesion molecules. Many of the upregulated genes are targets of interleukin 6 and nuclear factor kappa B regulation, suggesting a central role for these proteins in the response of tubular epithelial cells to HIV-1 infection. Analysis of kidneys from HIV-1 transgenic mice revealed upregulation of many of the proinflammatory genes identified in the microarray studies. These studies provide novel insights into the mechanisms by which HIV-1 infection of tubular epithelial cells leads to tubulointerstitial inflammation and progressive renal injury.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1525-4135
pubmed:author
pubmed:issnType
Print
pubmed:volume
42
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1-11
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:16763488-AIDS-Associated Nephropathy, pubmed-meshheading:16763488-Animals, pubmed-meshheading:16763488-Cell Adhesion Molecules, pubmed-meshheading:16763488-Cell Line, Tumor, pubmed-meshheading:16763488-Cytokines, pubmed-meshheading:16763488-Epithelial Cells, pubmed-meshheading:16763488-Fusion Proteins, gag-pol, pubmed-meshheading:16763488-Gene Expression Profiling, pubmed-meshheading:16763488-HIV Infections, pubmed-meshheading:16763488-HIV-1, pubmed-meshheading:16763488-Humans, pubmed-meshheading:16763488-Kidney, pubmed-meshheading:16763488-Kidney Tubules, pubmed-meshheading:16763488-Mice, pubmed-meshheading:16763488-Mice, Transgenic, pubmed-meshheading:16763488-Oligonucleotide Array Sequence Analysis, pubmed-meshheading:16763488-Proviruses, pubmed-meshheading:16763488-Reassortant Viruses, pubmed-meshheading:16763488-Time Factors, pubmed-meshheading:16763488-Up-Regulation, pubmed-meshheading:16763488-Vesicular stomatitis Indiana virus
pubmed:year
2006
pubmed:articleTitle
HIV-1 infection initiates an inflammatory cascade in human renal tubular epithelial cells.
pubmed:affiliation
Division of Nephrology, Mount Sinai School of Medicine, New York, NY 10029, USA. michael.ross@mssm.edu
pubmed:publicationType
Journal Article, Comparative Study, Research Support, N.I.H., Extramural