RGD Reference Report - Regression of warfarin-induced medial elastocalcinosis by high intake of vitamin K in rats. - Rat Genome Database

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Regression of warfarin-induced medial elastocalcinosis by high intake of vitamin K in rats.

Authors: Schurgers, LJ  Spronk, HM  Soute, BA  Schiffers, PM  DeMey, JG  Vermeer, C 
Citation: Schurgers LJ, etal., Blood. 2007 Apr 1;109(7):2823-31.
RGD ID: 2293588
Pubmed: PMID:17138823   (View Abstract at PubMed)
DOI: DOI:10.1182/blood-2006-07-035345   (Journal Full-text)

Arterial calcification (AC) is generally regarded as an independent risk factor for cardiovascular morbidity and mortality. Matrix Gla protein (MGP) is a potent inhibitor of AC, and its activity depends on vitamin K (VK). In rats, inactivation of MGP by treatment with the vitamin K antagonist warfarin leads to rapid calcification of the arteries. Here, we investigated whether preformed AC can be regressed by a VK-rich diet. Rats received a calcification-inducing diet containing both VK and warfarin (W&K). During a second 6-week period, animals were randomly assigned to receive either W&K (3.0 mg/g and 1.5 mg/g, subsequently), a diet containing a normal (5 microg/g) or high (100 microg/g) amount of VK (either K1 or K2). Increased aortic calcium concentration was observed in the group that continued to receive W&K and also in the group changed to the normal dose of VK and AC progressed. Both the VK-rich diets decreased the arterial calcium content by some 50%. In addition, arterial distensibility was restored by the VK-rich diet. Using MGP antibodies, local VK deficiency was demonstrated at sites of calcification. This is the first study in rats demonstrating that AC and the resulting decreased arterial distensibility are reversible by high-VK intake.



Phenotype Annotations    Click to see Annotation Detail View

Mammalian Phenotype

Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
MgpRatcalcified artery  IDA  RGD 
Objects Annotated

Genes (Rattus norvegicus)
Mgp  (matrix Gla protein)


Additional Information