| pubmed-article:18285351 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18285351 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:18285351 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:18285351 | lifeskim:mentions | umls-concept:C0024143 | lld:lifeskim |
| pubmed-article:18285351 | lifeskim:mentions | umls-concept:C0221198 | lld:lifeskim |
| pubmed-article:18285351 | lifeskim:mentions | umls-concept:C0333348 | lld:lifeskim |
| pubmed-article:18285351 | lifeskim:mentions | umls-concept:C1523116 | lld:lifeskim |
| pubmed-article:18285351 | lifeskim:mentions | umls-concept:C0450254 | lld:lifeskim |
| pubmed-article:18285351 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:18285351 | pubmed:dateCreated | 2008-4-21 | lld:pubmed |
| pubmed-article:18285351 | pubmed:abstractText | In vitro and in vivo experimental studies suggest that the transcription factor NF-kappaB plays a role in tubulointerstitial injury. We investigated possible cellular and molecular mechanisms involving NF-kappaB activation in the progression of tubulointerstitial lesions in human lupus nephritis (LN). Paraffin-embedded renal biopsies from 50 patients with LN and six control patients with minimal change disease (MCD) were examined by Southwestern histochemistry for in situ detection of active NF-kappaB and AP-1. Immunohistochemistry was performed to examine the expression of NF-kappaB, AP-1, and NF-kappaB regulatory proteins (IkappaB-alpha, p-IkappaB-alpha, and IKK-alpha proteins), as well as NF-kappaB and AP-1 downstream target proinflammatory molecules (ICAM-1, TNF-alpha, IL-1beta, IL-6, and GM-CSF) and NF-kappaB upstream signaling molecules (CD40 and CD40L). We observed extensive upregulation of activated NF-kappaB in renal tubular cells and interstitial cells, in parallel with overactivation of transcription factor AP-1 in LN, as compared with normal controls and MCD. Tubular expression of activated NF-kappaB correlated well with the degree of tubulointerstitial histopathological indices and/or renal function. Tubulointerstitial IKK-alpha expression was specifically upregulated in LN. IkappaB-alpha and p-IkappaB-alpha were detected only in interstitial cells in LN. Tubulointerstitial expression levels of NF-kappaB and AP-1 downstream inflammatory molecules and NF-kappaB upstream signaling molecules CD40 and CD40L were markedly enhanced in LN as compared with MCD or normal controls and were associated with tubulointerstitial histopathological indices and/or renal function. The results suggest that altered IKK-alpha expression and NF-kappaB activation along with AP-1 overexpression may play a pathogenic role in tubulointerstitial injury in human LN mediated through a network of downstream proinflammatory molecules. | lld:pubmed |
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| pubmed-article:18285351 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18285351 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18285351 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:18285351 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18285351 | pubmed:month | May | lld:pubmed |
| pubmed-article:18285351 | pubmed:issn | 0022-1554 | lld:pubmed |
| pubmed-article:18285351 | pubmed:author | pubmed-author:SinniahRajaR | lld:pubmed |
| pubmed-article:18285351 | pubmed:author | pubmed-author:ZhengLingL | lld:pubmed |
| pubmed-article:18285351 | pubmed:author | pubmed-author:HsuStephen... | lld:pubmed |
| pubmed-article:18285351 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:18285351 | pubmed:volume | 56 | lld:pubmed |
| pubmed-article:18285351 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18285351 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18285351 | pubmed:pagination | 517-29 | lld:pubmed |
| pubmed-article:18285351 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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