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The elastic lamellae of devitalized arteries calcify when incubated in serum: evidence for a serum calcification factor.

作者信息

Price Paul A, Chan Wai Si, Jolson Dawn M, Williamson Matthew K

机构信息

Division of Biological Sciences, University of California, San Diego, La Jolla, CA 92093-0368, USA.

出版信息

Arterioscler Thromb Vasc Biol. 2006 May;26(5):1079-85. doi: 10.1161/01.ATV.0000216406.44762.7c. Epub 2006 Mar 9.

Abstract

OBJECTIVE

To determine whether serum contains an activity that induces artery calcification.

METHODS AND RESULTS

The elastic lamellae of devitalized rat aortas calcify rapidly in rat or bovine serum, or in human serum provided [Pi] > or =2 mmol/L. This calcification is attributable to a potent serum calcification factor (SCF), one that causes devitalized aortas to calcify when incubated in DMEM containing as little as 1.5% serum but not in DMEM alone. The SCF that initiates medial elastin calcification has the same 50- to 150-kDa size and protease sensitivity as the SCF shown previously to initiate calcification of type I collagen. Our working hypothesis is that the same SCF initiates calcification of collagen and elastin, and that this SCF arises from sites of normal bone mineralization and, like alkaline phosphatase, is released into general circulation. The SCF does not initiate medial elastin calcification in living arteries, which suggests that vascular cells may prevent this calcification. This hypothesis is supported by the observations that living arteries secrete the calcification inhibitor matrix Gla protein (MGP); that inactivation of MGP with warfarin causes living arteries to calcify; and that addition of MGP to medium containing warfarin prevents this calcification.

CONCLUSIONS

The elastic lamellae of devitalized aortas calcify rapidly in serum.

摘要

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