| pubmed-article:16204413 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16204413 | lifeskim:mentions | umls-concept:C1522424 | lld:lifeskim |
| pubmed-article:16204413 | lifeskim:mentions | umls-concept:C0026336 | lld:lifeskim |
| pubmed-article:16204413 | lifeskim:mentions | umls-concept:C0078911 | lld:lifeskim |
| pubmed-article:16204413 | lifeskim:mentions | umls-concept:C0806036 | lld:lifeskim |
| pubmed-article:16204413 | lifeskim:mentions | umls-concept:C0205322 | lld:lifeskim |
| pubmed-article:16204413 | lifeskim:mentions | umls-concept:C1523116 | lld:lifeskim |
| pubmed-article:16204413 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:16204413 | pubmed:dateCreated | 2006-2-7 | lld:pubmed |
| pubmed-article:16204413 | pubmed:abstractText | Human immunodeficiency virus (HIV)-associated nephropathy (HIVAN) is caused, in part, by direct infection of kidney epithelial cells by HIV-1. In the spectrum of pathogenic host-virus interactions, abnormal activation or suppression of host transcription factors is common. NF-kappaB is a necessary host transcription factor for HIV-1 gene expression, and it has been shown that NF-kappaB activity is dysregulated in many naturally infected cell types. We show here that renal glomerular epithelial cells (podocytes) expressing the HIV-1 genome, similar to infected immune cells, also have a dysregulated and persistent activation of NF-kappaB. Although podocytes produce p50, p52, RelA, RelB, and c-Rel, electrophoretic mobility shift assays and immunocytochemistry showed a predominant nuclear accumulation of p50/RelA-containing NF-kappaB dimers in HIV-1-expressing podocytes compared with normal. In addition, the expression level of a transfected NF-kappaB reporter plasmid was significantly higher in HIVAN podocytes. The mechanism of NF-kappaB activation involved increased phosphorylation of IkappaBalpha, resulting in an enhanced turnover of the IkappaBalpha protein. There was no evidence for regulation by IkappaBbeta or the alternate pathway of NF-kappaB activation. Altered activation of this key host transcription factor likely plays a role in the well-described cellular phenotypic changes observed in HIVAN, such as proliferation. Studies with inhibitors of proliferation and NF-kappaB suggest that NF-kappaB activation may contribute to the proliferative mechanism in HIVAN. In addition, because NF-kappaB regulates many aspects of inflammation, this dysregulation may also contribute to disease severity and progression through regulation of proinflammatory processes in the kidney microenvironment. | lld:pubmed |
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| pubmed-article:16204413 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:16204413 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:16204413 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16204413 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:16204413 | pubmed:issn | 1931-857X | lld:pubmed |
| pubmed-article:16204413 | pubmed:author | pubmed-author:GraaflandHH | lld:pubmed |
| pubmed-article:16204413 | pubmed:author | pubmed-author:BruggemanLesl... | lld:pubmed |
| pubmed-article:16204413 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16204413 | pubmed:volume | 290 | lld:pubmed |
| pubmed-article:16204413 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16204413 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16204413 | pubmed:pagination | F657-65 | lld:pubmed |
| pubmed-article:16204413 | pubmed:dateRevised | 2011-9-26 | lld:pubmed |
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| pubmed-article:16204413 | pubmed:meshHeading | pubmed-meshheading:16204413... | lld:pubmed |
| pubmed-article:16204413 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16204413 | pubmed:articleTitle | Persistent NF-kappaB activation in renal epithelial cells in a mouse model of HIV-associated nephropathy. | lld:pubmed |
| pubmed-article:16204413 | pubmed:affiliation | Case Western Reserve University, MetroHealth Medical Center Campus, Rammelkamp Center R435, 2500 MetroHealth Drive, Cleveland, OH 44109, USA. | lld:pubmed |
| pubmed-article:16204413 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16204413 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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