pubmed-article:11292619 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11292619 | lifeskim:mentions | umls-concept:C0003009 | lld:lifeskim |
pubmed-article:11292619 | lifeskim:mentions | umls-concept:C1456820 | lld:lifeskim |
pubmed-article:11292619 | lifeskim:mentions | umls-concept:C0151650 | lld:lifeskim |
pubmed-article:11292619 | lifeskim:mentions | umls-concept:C1527148 | lld:lifeskim |
pubmed-article:11292619 | lifeskim:mentions | umls-concept:C1880177 | lld:lifeskim |
pubmed-article:11292619 | pubmed:issue | 5 | lld:pubmed |
pubmed-article:11292619 | pubmed:dateCreated | 2001-4-9 | lld:pubmed |
pubmed-article:11292619 | pubmed:abstractText | Angiotensin II upregulates tumor necrosis factor-alpha (TNF-alpha) in the rat kidney with unilateral ureteral obstruction (UUO). In a mouse model of UUO, we found that tubulointerstitial fibrosis is blunted when the TNF-alpha receptor, TNFR1, is functionally knocked out. In this study, we used mutant mice with UUO in which the angiotensin II receptor AT(1a) or the TNF-alpha receptors TNFR1 and TNFR2 were knocked out to elucidate interactions between the two systems. The contribution of both systems to renal fibrosis was assessed by treating TNFR1/TNFR2-double knockout (KO) mice with an angiotensin-converting enzyme inhibitor, enalapril. The increased interstitial volume (Vv(int)) in the C57BI/6 wild-type mouse was decreased in the AT(1a) KO from 32.8 +/- 4.0 to 21.0 +/- 3.7% (P < 0.005) or in the TNFR1/TNFR2 KO to 22.3 +/- 2.1% (P < 0.005). The Vv(int) of the TNFR1/TNFR2 KO was further decreased to 15.2 +/- 3.7% (P < 0.01) by enalapril compared with no treatment. The induction of TNF-alpha mRNA and transforming growth factor-beta1 (TGF-beta1) mRNA in the kidney with UUO was significantly blunted in the AT(1a) or TNFR1/TNFR2 KO mice compared with the wild-type mice. Treatment of the TNFR1/TNFR2 KO mouse with enalapril reduced both TNF-alpha and TGF-beta1 mRNA and their proteins to near normal levels. Also, alpha-smooth muscle actin expression and myofibroblast proliferation were significantly inhibited in the AT(1a) or TNFR1/TNFR2 KO mice, and they were further inhibited in enalapril-treated TNFR1/TNFR2 KO mice. Incapacitating the angiotensin II or the TNF-alpha systems individually leads to partial blunting of fibrosis. Incapacitating both systems, by using a combination of genetic and pharmacological means, further inhibited interstitial fibrosis and tubule atrophy in obstructive nephropathy. | lld:pubmed |
pubmed-article:11292619 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11292619 | pubmed:language | eng | lld:pubmed |
pubmed-article:11292619 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11292619 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:11292619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11292619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11292619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11292619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11292619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11292619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11292619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11292619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11292619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11292619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11292619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11292619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11292619 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11292619 | pubmed:month | May | lld:pubmed |
pubmed-article:11292619 | pubmed:issn | 1931-857X | lld:pubmed |
pubmed-article:11292619 | pubmed:author | pubmed-author:KlahrSS | lld:pubmed |
pubmed-article:11292619 | pubmed:author | pubmed-author:MorrisseyJJ | lld:pubmed |
pubmed-article:11292619 | pubmed:author | pubmed-author:GuyMM | lld:pubmed |
pubmed-article:11292619 | pubmed:author | pubmed-author:McCrackenRR | lld:pubmed |
pubmed-article:11292619 | pubmed:author | pubmed-author:LiapisHH | lld:pubmed |
pubmed-article:11292619 | pubmed:author | pubmed-author:TolleyTT | lld:pubmed |
pubmed-article:11292619 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11292619 | pubmed:volume | 280 | lld:pubmed |
pubmed-article:11292619 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11292619 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11292619 | pubmed:pagination | F777-85 | lld:pubmed |
pubmed-article:11292619 | pubmed:dateRevised | 2011-4-28 | lld:pubmed |
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pubmed-article:11292619 | pubmed:year | 2001 | lld:pubmed |
pubmed-article:11292619 | pubmed:articleTitle | Contributions of angiotensin II and tumor necrosis factor-alpha to the development of renal fibrosis. | lld:pubmed |
pubmed-article:11292619 | pubmed:affiliation | Departments of Internal Medicine, Washington University School of Medicine at Barnes-Jewish Hospital, 216 S. Kingshighway Blvd., St. Louis, Missouri 63110-1092, USA. | lld:pubmed |
pubmed-article:11292619 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:11292619 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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