Source:http://linkedlifedata.com/resource/pubmed/id/20847140
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
12
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pubmed:dateCreated |
2010-12-1
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pubmed:abstractText |
It is not clear whether interstitial fibroblasts or tubular epithelial cells are primarily responsible for the profibrotic effects of NF-?B activation during renal fibrogenesis. Here, we crossed mice carrying a conditional I?B dominant-negative transgene (I?BdN) with mice transgenic for cell-specific FSP1.Cre (FSP1(+) fibroblasts) or ?GT.Cre (proximal tubular epithelia) and challenged all progeny with unilateral ureteral obstruction. We determined NF-?B activation by nuclear localization of phosphorylated p65 ((p)p65) in renal tissues after 7 days. We observed inhibition of NF-?B activation in interstitial cells and tubular epithelia in obstructed kidneys of FSP1.Cre;I?BdN and ?GT.Cre;I?BdN mice, respectively, compared with I?BdN controls (P < 0.05). Deposition of extracellular matrix, however, was significantly lower in the obstructed kidneys of FSP1.Cre;I?BdN mice but not in ?GT.Cre;I?BdN mice (P < 0.05). In addition, levels of mRNA encoding the profibrotic PAI-1, fibronectin-EIIIA, and type I (?1) procollagen were significantly lower in obstructed kidneys of FSP1.Cre;I?BdN mice compared with ?GT.Cre;I?BdN mice (P < 0.05). Taken together, these data support a profibrotic role for fibroblasts, but not proximal tubular epithelial cells, in modulating NF-?B activation during renal fibrogenesis.
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pubmed:grant | |
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 |
Dec
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pubmed:issn |
1533-3450
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
21
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2047-52
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pubmed:dateRevised |
2011-1-10
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pubmed:meshHeading |
pubmed-meshheading:20847140-Animals,
pubmed-meshheading:20847140-Disease Models, Animal,
pubmed-meshheading:20847140-Fibroblasts,
pubmed-meshheading:20847140-Fibrosis,
pubmed-meshheading:20847140-Gene Expression Regulation,
pubmed-meshheading:20847140-I-kappa B Proteins,
pubmed-meshheading:20847140-Immunohistochemistry,
pubmed-meshheading:20847140-Kidney Diseases,
pubmed-meshheading:20847140-Male,
pubmed-meshheading:20847140-Mice,
pubmed-meshheading:20847140-Mice, Transgenic,
pubmed-meshheading:20847140-Polymerase Chain Reaction,
pubmed-meshheading:20847140-RNA, Messenger,
pubmed-meshheading:20847140-Random Allocation,
pubmed-meshheading:20847140-Reference Values,
pubmed-meshheading:20847140-Sensitivity and Specificity,
pubmed-meshheading:20847140-Transgenes
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pubmed:year |
2010
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pubmed:articleTitle |
Fibroblast expression of an I?B dominant-negative transgene attenuates renal fibrosis.
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pubmed:affiliation |
Department of Nephrology, Faculty of Medicine, Saitama Medical University, Saitama, Japan.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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