作者: Y Tintut , L L Demer , A Yochelis , A Garfinkel
DOI: 10.1088/1367-2630/10/5/055002
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摘要: Calcification and mineralization are fundamental physiological processes, yet the mechanisms of calcification, in trabecular bone calcified lesions atherosclerotic unclear. Recently, it was shown vitro experiments that vascular-derived mesenchymal stem cells can display self-organized patterns. These patterns were attributed to activator/inhibitor dynamics style Turing, with morphogenetic protein 2 acting as an activator, matrix GLA inhibitor. Motivated by this qualitative activator–inhibitor dynamics, we employ a prototype Gierer–Meinhardt model used context activator–inhibitor-based biological pattern formation. Through detailed analysis one two spatial dimensions, explore formation steady state patterns, including their dependence on initial conditions. range from localized holes labyrinths peaks, or other words, dense sparse activator distributions (respectively). We believe understanding wide spectrum discussed here is prerequisite biochemical control. The suggest therapeutic strategies applicable arteries (where pathological) regeneration (recapitulating normal development).