Truncated amelogenin and LRAP transgenes improve Amelx null mouse enamel.
Truncated amelogenin and LRAP transgenes improve Amelx null mouse enamel.
复制标题
截短的牙釉蛋白和 LRAP 转基因改善了 Amelx 缺失小鼠的牙釉质。
DOI:
10.1016/j.matbio.2015.11.005
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发表时间:
2016
期刊:
影响因子:
--
通讯作者:
Pugach,MeganK
中科院分区:
文献类型:
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作者:
Xia,Yan;Ren,Anna;Pugach,MeganK
Amelogenin is the most abundant enamel protein involved in enamel mineralization. Our goal was to determine whether all three regions of amelogenin (N-terminus, C-terminus, central core) are required for enamel formation. Amelogenin RNA is alternatively spliced, resulting in at least 16 different amelogenin isoforms in mice, with M180 and LRAP expressed most abundantly. Soon after secretion by ameloblasts, M180 is cleaved by MMP20 resulting in C-terminal truncated (CTRNC) amelogenin. We aimed to determine whether the 2 transgenes (Tg), LRAP and CTRNC together, can improve LRAPTg/Amelx−/− and CTRNCTg/Amelx−/− enamel thickness and prism organization, which were not rescued inAmelx−/− enamel. We generated CTRNCTg/LRAPTg/Amelx−/− mice and analyzed developing and mature incisor and molar enamel histologically, by microCT, SEM and microhardness testing. CTRNCTg and LRAPTg overexpression together significantly improved the enamel phenotype of LRAPTg/Amelx−/− and CTRNCTg/Amelx−/− mouse enamel, however enamel microhardness was recovered only when M180Tg was expressed, alone or with LRAPTg. We determined that both LRAP and CTRNC, which together express all three regions of the amelogenin protein (N-terminus, C-terminus and hydrophobic core) contribute to the final enamel thickness and prism organization in mice.