| pubmed-article:19286962 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19286962 | lifeskim:mentions | umls-concept:C0027051 | lld:lifeskim |
| pubmed-article:19286962 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:19286962 | lifeskim:mentions | umls-concept:C0026565 | lld:lifeskim |
| pubmed-article:19286962 | lifeskim:mentions | umls-concept:C0031437 | lld:lifeskim |
| pubmed-article:19286962 | lifeskim:mentions | umls-concept:C0205217 | lld:lifeskim |
| pubmed-article:19286962 | lifeskim:mentions | umls-concept:C1419781 | lld:lifeskim |
| pubmed-article:19286962 | lifeskim:mentions | umls-concept:C0857121 | lld:lifeskim |
| pubmed-article:19286962 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:19286962 | pubmed:dateCreated | 2009-5-4 | lld:pubmed |
| pubmed-article:19286962 | pubmed:abstractText | S100A1 is a small Ca(2+)-binding protein expressed in the myocardium and blood vessels that is downregulated in the diseased heart and plays a role in the regulation of cardiac muscle Ca(2+) homeostasis and contractility. To understand its physiological role under basal conditions and after myocardial infarction (MI), we used a mouse strain with targeted deletion of the S100A1 gene [S100A1 knockout (KO) mice]. We compared 49 wild-type (WT) and 56 S100A1 KO mice (6-8 wk old) over 28 days after MI with sham-operated controls. We also examined the effect of S100A1 deficiency on vascular function of isolated blood vessels. S100A1 KO mice demonstrated worse survival compared with WT mice (21% vs. 69%, respectively, P < 0.001). Hemodynamic evaluation revealed a higher mean arterial pressure (MAP) in sham-operated KO animals compared with WT animals (99 +/- 4 vs. 77 +/- 3 mmHg, respectively, P < 0.001) that persisted in both groups after MI (86 +/- 2 vs. 66 +/- 4 mmHg, respectively, P < 0.001). Sham-operated male S100A1 KO mice had higher MAP than female KO mice (122 +/- 5 vs. 93 +/- 3 mmHg, respectively P < 0.05) and reduced survival after MI (4% vs. 27%, respectively, P < 0.05). In isolated aortas and mesenteric arteries, ACh-evoked vasodilatation in KO mice was significantly reduced compared with WT mice (P < 0.05). Nitric oxide production was reduced in endothelial cells isolated from KO mice. Thus, absence of S100A1 results in acute functional impairment and high mortality after MI associated with a gender-specific hypertensive phenotype. S100A1 appears to play a role in the endothelium-dependent regulation of blood pressure. | lld:pubmed |
| pubmed-article:19286962 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19286962 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19286962 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:19286962 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19286962 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19286962 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19286962 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19286962 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19286962 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19286962 | pubmed:month | May | lld:pubmed |
| pubmed-article:19286962 | pubmed:issn | 0363-6135 | lld:pubmed |
| pubmed-article:19286962 | pubmed:author | pubmed-author:ParkerThomas... | lld:pubmed |
| pubmed-article:19286962 | pubmed:author | pubmed-author:Leong-PoiHowa... | lld:pubmed |
| pubmed-article:19286962 | pubmed:author | pubmed-author:VermaSubodhS | lld:pubmed |
| pubmed-article:19286962 | pubmed:author | pubmed-author:PourdjabbarAl... | lld:pubmed |
| pubmed-article:19286962 | pubmed:author | pubmed-author:Teichert-Kuli... | lld:pubmed |
| pubmed-article:19286962 | pubmed:author | pubmed-author:QuanAdrianA | lld:pubmed |
| pubmed-article:19286962 | pubmed:author | pubmed-author:DesjardinsJea... | lld:pubmed |
| pubmed-article:19286962 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:19286962 | pubmed:volume | 296 | lld:pubmed |
| pubmed-article:19286962 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19286962 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19286962 | pubmed:pagination | H1457-65 | lld:pubmed |
| pubmed-article:19286962 | pubmed:meshHeading | pubmed-meshheading:19286962... | lld:pubmed |
| pubmed-article:19286962 | pubmed:meshHeading | pubmed-meshheading:19286962... | lld:pubmed |
| pubmed-article:19286962 | pubmed:meshHeading | pubmed-meshheading:19286962... | lld:pubmed |
| pubmed-article:19286962 | pubmed:meshHeading | pubmed-meshheading:19286962... | lld:pubmed |
| pubmed-article:19286962 | pubmed:meshHeading | pubmed-meshheading:19286962... | lld:pubmed |
| pubmed-article:19286962 | pubmed:meshHeading | pubmed-meshheading:19286962... | lld:pubmed |
| pubmed-article:19286962 | pubmed:meshHeading | pubmed-meshheading:19286962... | lld:pubmed |
| pubmed-article:19286962 | pubmed:meshHeading | pubmed-meshheading:19286962... | lld:pubmed |
| pubmed-article:19286962 | pubmed:meshHeading | pubmed-meshheading:19286962... | lld:pubmed |
| pubmed-article:19286962 | pubmed:meshHeading | pubmed-meshheading:19286962... | lld:pubmed |
| pubmed-article:19286962 | pubmed:meshHeading | pubmed-meshheading:19286962... | lld:pubmed |
| pubmed-article:19286962 | pubmed:meshHeading | pubmed-meshheading:19286962... | lld:pubmed |
| pubmed-article:19286962 | pubmed:meshHeading | pubmed-meshheading:19286962... | lld:pubmed |
| pubmed-article:19286962 | pubmed:meshHeading | pubmed-meshheading:19286962... | lld:pubmed |
| pubmed-article:19286962 | pubmed:meshHeading | pubmed-meshheading:19286962... | lld:pubmed |
| pubmed-article:19286962 | pubmed:meshHeading | pubmed-meshheading:19286962... | lld:pubmed |
| pubmed-article:19286962 | pubmed:meshHeading | pubmed-meshheading:19286962... | lld:pubmed |
| pubmed-article:19286962 | pubmed:meshHeading | pubmed-meshheading:19286962... | lld:pubmed |
| pubmed-article:19286962 | pubmed:meshHeading | pubmed-meshheading:19286962... | lld:pubmed |
| pubmed-article:19286962 | pubmed:meshHeading | pubmed-meshheading:19286962... | lld:pubmed |
| pubmed-article:19286962 | pubmed:meshHeading | pubmed-meshheading:19286962... | lld:pubmed |
| pubmed-article:19286962 | pubmed:meshHeading | pubmed-meshheading:19286962... | lld:pubmed |
| pubmed-article:19286962 | pubmed:meshHeading | pubmed-meshheading:19286962... | lld:pubmed |
| pubmed-article:19286962 | pubmed:meshHeading | pubmed-meshheading:19286962... | lld:pubmed |
| pubmed-article:19286962 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19286962 | pubmed:articleTitle | Lack of S100A1 in mice confers a gender-dependent hypertensive phenotype and increased mortality after myocardial infarction. | lld:pubmed |
| pubmed-article:19286962 | pubmed:affiliation | Division of Cardiology, St. Michael's Hospital, University of Toronto, 30 Bond St., Rm. 6-044, Queen Wing, Toronto, ON, Canada M5B 1W8. | lld:pubmed |
| pubmed-article:19286962 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19286962 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:19286962 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:20193 | entrezgene:pubmed | pubmed-article:19286962 | lld:entrezgene |
| http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:19286962 | lld:entrezgene |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:19286962 | lld:pubmed |
