Source:http://linkedlifedata.com/resource/pubmed/id/21281809
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions |
umls-concept:C0007634,
umls-concept:C0022661,
umls-concept:C0025914,
umls-concept:C0026336,
umls-concept:C0026809,
umls-concept:C0026844,
umls-concept:C0205098,
umls-concept:C0221464,
umls-concept:C0392747,
umls-concept:C0403447,
umls-concept:C1135918,
umls-concept:C1318444,
umls-concept:C1517945,
umls-concept:C1533591,
umls-concept:C2610433
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| pubmed:issue |
2
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| pubmed:dateCreated |
2011-2-1
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| pubmed:abstractText |
Arterial medial calcification (AMC), a hallmark of vascular disease in uremic patients, is highly correlated with serum phosphate levels and cardiovascular mortality. To determine the mechanisms of AMC, mice were made uremic by partial right-side renal ablation (week 0), followed by left-side nephrectomy at week 2. At 3 weeks, mice were switched to a high-phosphate diet, and various parameters of disease progression were examined over time. Serum phosphate, calcium, and fibroblast growth factor 23 (FGF-23) were up-regulated as early as week 4. Whereas serum phosphate and calcium levels declined to normal by 10 weeks, FGF-23 levels remained elevated through 16 weeks, consistent with an increased phosphate load. Elastin turnover and vascular smooth muscle cell (VSMC) phenotype change were early events, detected by week 4 and before AMC. Both AMC and VSMC loss were significantly elevated by week 8. Matrix metalloprotease 2 (MMP-2) and cathepsin S were present at baseline and were significantly elevated at weeks 8 and 12. In contrast, MMP-9 was not up-regulated until week 12. These findings over time suggest that VSMC phenotype change and VSMC loss (early phosphate-dependent events) may be necessary and sufficient to promote AMC in uremic mice fed a high-phosphate diet, whereas elastin degradation might be necessary but is not sufficient to induce AMC (because elastin degradation occurred also in uremic mice on a normal-phosphate diet, but they did not develop AMC).
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Feb
|
| pubmed:issn |
1525-2191
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| pubmed:author | |
| pubmed:copyrightInfo |
Copyright © 2011 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.
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| pubmed:issnType |
Electronic
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| pubmed:volume |
178
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
764-73
|
| pubmed:meshHeading |
pubmed-meshheading:21281809-Animals,
pubmed-meshheading:21281809-Calcinosis,
pubmed-meshheading:21281809-Cell Death,
pubmed-meshheading:21281809-Diet,
pubmed-meshheading:21281809-Disease Models, Animal,
pubmed-meshheading:21281809-Disease Progression,
pubmed-meshheading:21281809-Elastin,
pubmed-meshheading:21281809-Enzyme Activation,
pubmed-meshheading:21281809-Immunohistochemistry,
pubmed-meshheading:21281809-Kidney Failure, Chronic,
pubmed-meshheading:21281809-Matrix Metalloproteinases,
pubmed-meshheading:21281809-Mice,
pubmed-meshheading:21281809-Muscle, Smooth, Vascular,
pubmed-meshheading:21281809-Myocytes, Smooth Muscle,
pubmed-meshheading:21281809-Phenotype,
pubmed-meshheading:21281809-Phosphates,
pubmed-meshheading:21281809-Time Factors,
pubmed-meshheading:21281809-Tunica Media,
pubmed-meshheading:21281809-Uremia
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| pubmed:year |
2011
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| pubmed:articleTitle |
Elastin degradation and vascular smooth muscle cell phenotype change precede cell loss and arterial medial calcification in a uremic mouse model of chronic kidney disease.
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| pubmed:affiliation |
Department of Bioengineering, University of Washington, Seattle, Washington, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
|