| pubmed-article:19287096 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19287096 | lifeskim:mentions | umls-concept:C0175677 | lld:lifeskim |
| pubmed-article:19287096 | lifeskim:mentions | umls-concept:C0332307 | lld:lifeskim |
| pubmed-article:19287096 | lifeskim:mentions | umls-concept:C0021368 | lld:lifeskim |
| pubmed-article:19287096 | lifeskim:mentions | umls-concept:C0022646 | lld:lifeskim |
| pubmed-article:19287096 | lifeskim:mentions | umls-concept:C0022663 | lld:lifeskim |
| pubmed-article:19287096 | lifeskim:mentions | umls-concept:C0027697 | lld:lifeskim |
| pubmed-article:19287096 | lifeskim:mentions | umls-concept:C0034787 | lld:lifeskim |
| pubmed-article:19287096 | lifeskim:mentions | umls-concept:C0443146 | lld:lifeskim |
| pubmed-article:19287096 | lifeskim:mentions | umls-concept:C0591833 | lld:lifeskim |
| pubmed-article:19287096 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:19287096 | pubmed:dateCreated | 2009-4-2 | lld:pubmed |
| pubmed-article:19287096 | pubmed:abstractText | Studies in humans and animal models indicate a key contribution of angiotensin II to the pathogenesis of glomerular diseases. To examine the role of type 1 angiotensin (AT1) receptors in glomerular inflammation associated with autoimmune disease, we generated MRL-Faslpr/lpr (lpr) mice lacking the major murine type 1 angiotensin receptor (AT1A); lpr mice develop a generalized autoimmune disease with glomerulonephritis that resembles SLE. Surprisingly, AT1A deficiency was not protective against disease but instead substantially accelerated mortality, proteinuria, and kidney pathology. Increased disease severity was not a direct effect of immune cells, since transplantation of AT1A-deficient bone marrow did not affect survival. Moreover, autoimmune injury in extrarenal tissues, including skin, heart, and joints, was unaffected by AT1A deficiency. In murine systems, there is a second type 1 angiotensin receptor isoform, AT1B, and its expression is especially prominent in the renal glomerulus within podocytes. Further, expression of renin was enhanced in kidneys of AT1A-deficient lpr mice, and they showed evidence of exaggerated AT1B receptor activation, including substantially increased podocyte injury and expression of inflammatory mediators. Administration of losartan, which blocks all type 1 angiotensin receptors, reduced markers of kidney disease, including proteinuria, glomerular pathology, and cytokine mRNA expression. Since AT1A-deficient lpr mice had low blood pressure, these findings suggest that activation of type 1 angiotensin receptors in the glomerulus is sufficient to accelerate renal injury and inflammation in the absence of hypertension. | lld:pubmed |
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| pubmed-article:19287096 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19287096 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19287096 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:19287096 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:19287096 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19287096 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:19287096 | pubmed:issn | 1558-8238 | lld:pubmed |
| pubmed-article:19287096 | pubmed:author | pubmed-author:ChenBenny JBJ | lld:pubmed |
