Spontaneous calcification of arteries and cartilage in mice lacking matrix GLA protein View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1997-03

AUTHORS

G Luo, P Ducy, M D McKee, G J Pinero, E Loyer, R R Behringer, G Karsenty

ABSTRACT

Calcification of the extracellular matrix (ECM) can be physiological or pathological. Physiological calcification occurs in bone when the soft ECM is converted into a rigid material capable of sustaining mechanical force; pathological calcification can occur in arteries and cartilage and other soft tissues. No molecular determinant regulating ECM calcification has yet been identified. A candidate molecule is matrix GLA protein (Mgp), a mineral-binding ECM protein synthesized by vascular smooth-muscle cells and chondrocytes, two cell types that produce an uncalcified ECM. Mice that lack Mgp develop to term but die within two months as a result of arterial calcification which leads to blood-vessel rupture. Chondrocytes that elaborate a typical cartilage matrix can be seen in the affected arteries. Mgp-deficient mice additionally exhibit inappropriate calcification of various cartilages, including the growth plate, which eventually leads to short stature, osteopenia and fractures. These results indicate that ECM calcification must be actively inhibited in soft tissues. To our knowledge, Mgp is the first inhibitor of calcification of arteries and cartilage to be characterized in vivo. More... »

PAGES

78

Journal

TITLE

Nature

ISSUE

6620

VOLUME

386

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/386078a0

    DOI

    http://dx.doi.org/10.1038/386078a0

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1008386602

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/9052783


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