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dc.contributor.authorHoward Hsuen_US
dc.contributor.authorAntonio Artiguesen_US
dc.contributor.authorMaria Villaren_US
dc.date.accessioned2009-05-05T16:14:39Z
dc.date.available2009-05-05T16:14:39Z
dc.date.issued2006-10-16en_US
dc.identifier.citationHoward Hsu;Antonio Artigues;Maria Villar: Induction of calcification by serum depletion in cell culture: a model for focal calcification in aortas related to atherosclerosis. Lipids Health Dis 2008, 7(1):2.en_US
dc.identifier.urihttp://hdl.handle.net/2271/600en_US
dc.description.abstractBACKGROUND:Since aortic calcification has been shown to initiate in the lower zone of well-thickened plaques (LZP) adjacent to the aortic media of rabbits fed supplemental cholesterol diets, a restricted supply of serum to vascular cells could play a role in vascular calcification. This study was designed to use a cell culture model to support this hypothesis.RESULTS:Rabbit aortic smooth muscle cells were grown to confluence in a culture media containing 10 % fetal bovine serum (FBS). The confluent cells were then exposed to the media for 2 hrs with or without serum at a Ca × P ion product range of 4.5 9.4 mM2. In contrast to the cells cultured in the presence of FBS, confluent cells in its absence displayed marked mineral-positive alizarin red staining and infrared absorption of mineral phosphate. A kinetic parameter C1/2 was used to designate the concentration of serum or its protein constituents needed to reduce the deposition of Ca and P by half. The C1/2 for FBS and rabbit serum was 0.04 0.07 % The C1/2 value for rabbit serum proteins was 13.5 µg/ml corresponding to the protein concentration in 0.06 % of serum. This C1/2 was markedly smaller than 86.2 µg/ml for bovine serum albumin present in 0.37 % serum (p < 0.05). Serum depletion also caused marked membrane translocation as evidenced through a specific apoptosis dye uptake by cells. The proteomic analysis of calcifying vesicles, which can be released by serum depletion, revealed several calcification-related proteins.CONCLUSION:The aortic smooth muscle cell culture model suggests that serum depletion may play a role in the initiation of aortic calcification. The serum exhibits remarkable ability to inhibit cell-mediated calcification.en_US
dc.languageenen_US
dc.language.isoen_USen_US
dc.publisherBioMedCentralen_US
dc.relation.isversionofhttp://www.lipidworld.com/content/7/1/2en_US
dc.relation.hasversionhttp://www.biomedcentral.com/content/pdf/1476-511X-7-2.pdfen_US
dc.rightsThis is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.en_US
dc.rights.urihttp://creativecommons.org/licenses/by/2.0en_US
dc.subject.meshAnimalsen_US
dc.subject.meshAorta, Thoracic/metabolism/ pathologyen_US
dc.subject.meshAortic Diseases/etiology/metabolism/pathologyen_US
dc.subject.meshBiological Markers/metabolismen_US
dc.subject.meshCalcinosis/metabolism/ pathologyen_US
dc.subject.meshCholesterol, Dietary/adverse effects/ metabolismen_US
dc.subject.meshCholesterol, LDL/ metabolismen_US
dc.subject.meshCoronary Artery Disease/etiology/metabolism/pathologyen_US
dc.subject.meshCytoplasmic Vesicles/metabolism/ pathologyen_US
dc.subject.meshDiet, Atherogenicen_US
dc.subject.meshDietary Supplements/adverse effectsen_US
dc.subject.meshHypercholesterolemia/blooden_US
dc.subject.meshMaleen_US
dc.subject.meshMicrosomes/metabolism/pathologyen_US
dc.subject.meshRabbitsen_US
dc.subject.meshTunica Intima/metabolism/ pathologyen_US
dc.titleInduction of calcification by serum depletion in cell culture: a model for focal calcification in aortas related to atherosclerosisen_US
dc.typeArticleen_US
dc.identifier.doi10.1186/1476-511X-7-2en_US
dc.identifier.pmid17042957en_US
dc.rights.accessrightsopenAccessen_US
dc.date.captured2009-04-27en_US


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This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Except where otherwise noted, this item's license is described as: This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.