Bronckers A L J J, Lyaruu D, Jalali R, Medina J F, Zandieh-Doulabi B, DenBesten P K
Department of Oral Cell Biology, Academic Centre for Dentistry Amsterdam, University of Amsterdam, and MOVE Research Institute, VU University Amsterdam, Amsterdam, Netherlands
Department of Oral Cell Biology, Academic Centre for Dentistry Amsterdam, University of Amsterdam, and MOVE Research Institute, VU University Amsterdam, Amsterdam, Netherlands.
J Dent Res. 2015 Dec;94(12):1740-7. doi: 10.1177/0022034515606900. Epub 2015 Sep 24.
Ameloblasts express transmembrane proteins for transport of mineral ions and regulation of pH in the enamel space. Two major transporters recently identified in ameloblasts are the Na(+)K(+)-dependent calcium transporter NCKX4 and the Na(+)-dependent HPO4 (2-) (Pi) cotransporter NaPi-2b. To regulate pH, ameloblasts express anion exchanger 2 (Ae2a,b), chloride channel Cftr, and amelogenins that can bind protons. Exposure to fluoride or null mutation of Cftr, Ae2a,b, or Amelx each results in formation of hypomineralized enamel. We hypothesized that enamel hypomineralization associated with disturbed pH regulation results from reduced ion transport by NCKX4 and NaPi-2b. This was tested by correlation analyses among the levels of Ca, Pi, Cl, Na, and K in forming enamel of mice with null mutation of Cftr, Ae2a,b, and Amelx, according to quantitative x-ray electron probe microanalysis. Immunohistochemistry, polymerase chain reaction analysis, and Western blotting confirmed the presence of apical NaPi-2b and Nckx4 in maturation-stage ameloblasts. In wild-type mice, K levels in enamel were negatively correlated with Ca and Cl but less negatively or even positively in fluorotic enamel. Na did not correlate with P or Ca in enamel of wild-type mice but showed strong positive correlation in fluorotic and nonfluorotic Ae2a,b- and Cftr-null enamel. In hypomineralizing enamel of all models tested, 1) Cl(-) was strongly reduced; 2) K(+) and Na(+) accumulated (Na(+) not in Amelx-null enamel); and 3) modulation was delayed or blocked. These results suggest that a Na(+)K(+)-dependent calcium transporter (likely NCKX4) and a Na(+)-dependent Pi transporter (potentially NaPi-2b) located in ruffle-ended ameloblasts operate in a coordinated way with the pH-regulating machinery to transport Ca(2+), Pi, and bicarbonate into maturation-stage enamel. Acidification and/or associated physicochemical/electrochemical changes in ion levels in enamel fluid near the apical ameloblast membrane may reduce the transport activity of mineral transporters, which results in hypomineralization.
成釉细胞表达跨膜蛋白,用于在釉质间隙中运输矿物质离子并调节pH值。最近在成釉细胞中发现的两种主要转运蛋白是钠钾依赖性钙转运蛋白NCKX4和钠依赖性磷酸氢根(2-)(Pi)协同转运蛋白NaPi-2b。为了调节pH值,成釉细胞表达阴离子交换蛋白2(Ae2a,b)、氯离子通道Cftr和能结合质子的釉原蛋白。暴露于氟化物或Cftr、Ae2a,b或Amelx的无效突变均会导致形成矿化不足的釉质。我们推测,与pH调节紊乱相关的釉质矿化不足是由NCKX4和NaPi-2b的离子转运减少所致。根据定量X射线电子探针显微分析,通过对Cftr、Ae2a,b和Amelx无效突变小鼠正在形成的釉质中钙、磷、氯、钠和钾水平进行相关性分析来验证这一推测。免疫组织化学、聚合酶链反应分析和蛋白质印迹证实了成熟阶段成釉细胞顶端存在NaPi-2b和Nckx4。在野生型小鼠中,釉质中的钾水平与钙和氯呈负相关,但在氟斑牙釉质中负相关性较小甚至呈正相关。在野生型小鼠的釉质中,钠与磷或钙不相关,但在氟斑牙和非氟斑牙的Ae2a,b和Cftr无效突变釉质中呈强正相关。在所有测试模型的矿化不足的釉质中,1)氯离子(Cl-)大幅减少;2)钾离子(K+)和钠离子(Na+)积累(在Amelx无效突变釉质中钠离子不积累);3)调节延迟或受阻。这些结果表明,位于皱褶末端成釉细胞中的钠钾依赖性钙转运蛋白(可能是NCKX4)和钠依赖性磷转运蛋白(可能是NaPi-2b)与pH调节机制协同作用,将钙离子(Ca2+)、磷离子(Pi)和碳酸氢根转运到成熟阶段的釉质中。成釉细胞顶端膜附近釉质液中离子水平的酸化和/或相关的物理化学/电化学变化可能会降低矿物质转运蛋白的转运活性,从而导致矿化不足。