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. 2019 Apr 16;6:49. doi: 10.3389/fcvm.2019.00049

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Copyright © 2019 Goto, Rogers, Blaser, Higashi, Lee, Schlotter, Body, Aikawa, Singh and Aikawa.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Model of OM and PM induction of VIC calcification, including passage-dependent effects. At early passage, some but not all VICs isolated from human calcific aortic valve disease donor tissues can have relatively high tissue non-specific alkaline phosphatase activity (TNAP), which is reduced by culture passaging. TNAP hydrolyzes β-glycerophosphate to inorganic phosphate that is incorporated into nascent hydroxyapatite crystals forming cardiovascular calcifications along with reducing the calcification inhibitor, pyrophosphate, making OM VIC calcification donor- and TNAP-dependent. Pro-calcifying media containing inorganic phosphate does not require TNAP to form hydroxyapatite crystals, and as such PM calcification is not suppressed by passage-dependent reductions in TNAP activity.