Source:http://linkedlifedata.com/resource/pubmed/id/19286962
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
5
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| pubmed:dateCreated |
2009-5-4
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| 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.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Anesthetics,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide,
http://linkedlifedata.com/resource/pubmed/chemical/S100 Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/S100A1 protein,
http://linkedlifedata.com/resource/pubmed/chemical/Xylazine
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| pubmed:status |
MEDLINE
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| pubmed:month |
May
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| pubmed:issn |
0363-6135
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
296
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
H1457-65
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| pubmed:meshHeading |
pubmed-meshheading:19286962-Anesthetics,
pubmed-meshheading:19286962-Animals,
pubmed-meshheading:19286962-Aorta,
pubmed-meshheading:19286962-Blood Pressure,
pubmed-meshheading:19286962-Disease Models, Animal,
pubmed-meshheading:19286962-Endothelium, Vascular,
pubmed-meshheading:19286962-Female,
pubmed-meshheading:19286962-Genotype,
pubmed-meshheading:19286962-Hypertension,
pubmed-meshheading:19286962-Male,
pubmed-meshheading:19286962-Mesenteric Arteries,
pubmed-meshheading:19286962-Mice,
pubmed-meshheading:19286962-Mice, Inbred C57BL,
pubmed-meshheading:19286962-Mice, Knockout,
pubmed-meshheading:19286962-Myocardial Contraction,
pubmed-meshheading:19286962-Myocardial Infarction,
pubmed-meshheading:19286962-Myocardium,
pubmed-meshheading:19286962-Nitric Oxide,
pubmed-meshheading:19286962-Phenotype,
pubmed-meshheading:19286962-S100 Proteins,
pubmed-meshheading:19286962-Sex Factors,
pubmed-meshheading:19286962-Time Factors,
pubmed-meshheading:19286962-Vasodilation,
pubmed-meshheading:19286962-Xylazine
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| pubmed:year |
2009
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| pubmed:articleTitle |
Lack of S100A1 in mice confers a gender-dependent hypertensive phenotype and increased mortality after myocardial infarction.
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| 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.
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| pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
|