A neo cassette replaces the promoter and exons 1-4 of the matrix Gla protein (Mgp) gene, abolishing gene expression. Homozygotes are viable but die within two months of age due to aortic rupture. Normally, MGP is present in bone, heart, kidney, lung, aorta and other vasculature, and can function as an arterial calcification inhibitor. These Mgpm1 mice develop vascular calcification involving ectopic bone formation and osteochondrogenic differentiation in multipotent cells in the vascular media and endothelium. Lack of MGP in the endothelium triggers endothelial-mesenchymal transitions, which allow the endothelial cells to contribute cells to the vascular calcification. Mgpm1 mice also exhibit abnormal calcification patterns in cartilage and the bone growth plate, which eventually leads to short stature and osteopenia. The lack of MGP also causes arteriovenous malformations (AVMs) in the lungs, kidneys and brain. The AVMs in the lungs and kidneys are associated with abnormal cell differentiation in the endothelium.

The promoter and exons 1-4 of the matrix Gla protein (Mgp) gene has been disrupted in these mice. Homozygous mice develop vascular calcification involving ectopic bone formation and osteochondrogenic differentiation in multipotent cells in the vascular media and endothelium. These Mgpm1 mice may be useful for studying arterial calcification.

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