Defective enamel and bone development in sodium-dependent citrate transporter (NaCT) Slc13a5 deficient mice.
Defective enamel and bone development in sodium-dependent citrate transporter (NaCT) Slc13a5 deficient mice.
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DOI：
10.1371/journal.pone.0175465
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发表时间：
2017
期刊：
影响因子：
3.7
通讯作者：
Rong JX
中科院分区：
文献类型：
--
作者：
Irizarry AR;Yan G;Zeng Q;Lucchesi J;Hamang MJ;Ma YL;Rong JX
人们越来越认识到柠檬酸在包括牙齿和骨骼在内的矿化组织的生物力学特性中所起的重要作用。然而，柠檬酸在这些组织中的来源还没有得到很好的确定，也没有研究柠檬酸对牙齿形成和成骨的调节作用。在这里，研究了13周龄和32周龄缺钠柠檬酸转运蛋白(NACT)SLc13a5缺陷的C57BL/6小鼠的牙齿和骨骼表型。Scl13a5缺乏导致牙齿发育缺陷，其特征是缺乏成熟的釉质，形成异常的釉质基质，釉质器官上皮异常发育和增殖，并随着年龄的增长而发展。这些异常与脆弱的牙齿有关，可能有牙齿脓肿的倾向。成熟牙釉质的缺乏与成釉发育不全相一致。此外，SLC13a5缺乏导致13周龄小鼠的骨密度下降和骨形成障碍，但在老年小鼠中没有。这些发现揭示了柠檬酸盐和SLC13a5在牙齿和骨骼的发育和功能中潜在的重要作用。
There has been growing recognition of the essential roles of citrate in biomechanical properties of mineralized tissues, including teeth and bone. However, the sources of citrate in these tissues have not been well defined, and the contribution of citrate to the regulation of odontogenesis and osteogenesis has not been examined. Here, tooth and bone phenotypes were examined in sodium-dependent citrate transporter (NaCT) Slc13a5 deficient C57BL/6 mice at 13 and 32 weeks of age. Slc13a5 deficiency led to defective tooth development, characterized by absence of mature enamel, formation of aberrant enamel matrix, and dysplasia and hyperplasia of the enamel organ epithelium that progressed with age. These abnormalities were associated with fragile teeth with a possible predisposition to tooth abscesses. The lack of mature enamel was consistent with amelogenesis imperfecta. Furthermore, Slc13a5 deficiency led to decreased bone mineral density and impaired bone formation in 13-week-old mice but not in older mice. The findings revealed the potentially important role of citrate and Slc13a5 in the development and function of teeth and bone.