The Role of Na:K:2Cl Cotransporter 1 (NKCC1/SLC12A2) in Dental Epithelium during Enamel Formation in Mice.
The Role of Na:K:2Cl Cotransporter 1 (NKCC1/SLC12A2) in Dental Epithelium during Enamel Formation in Mice.
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DOI：
10.3389/fphys.2017.00924
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发表时间：
2017
影响因子：
4
通讯作者：
Bronckers A
中科院分区：
文献类型：
--
作者：
Jalali R;Lodder JC;Zandieh-Doulabi B;Micha D;Melvin JE;Catalan MA;Mansvelder HD;DenBesten P;Bronckers A
钠 - 钾 - 2氯协同转运蛋白（NKCCs）属于阳离子耦合氯转运蛋白的SLC12A家族。我们研究了产生釉质的小鼠成釉细胞是否表达NKCCs。通过实时定量聚合酶链反应（RT - qPCR）在小鼠牙上皮中鉴定出Nkcc1的转录本，并且NKCC1蛋白免疫定位在外釉上皮和乳头层，但不在成釉细胞层。在Nkcc1基因缺失小鼠的切牙中，成熟晚期的成釉细胞紊乱、变短，并且与野生型对照相比，釉质的矿物质密度降低了10%。在Nkcc1基因缺失的釉质器官中，缝隙连接蛋白连接蛋白43、钠依赖性碳酸氢盐协同转运蛋白e1（NBCe1）以及氯依赖性碳酸氢盐交换蛋白SLC26A3和SLC26A6的蛋白质水平上调，而成熟成釉细胞中主要的钾、钠依赖性钙转运蛋白NCKX4/SLC24A4的水平略有下调。对大鼠成釉细胞样HAT - 7细胞进行的全细胞电压钳研究表明，布美他尼增加了传导外向电流的离子通道活性。布美他尼还降低了HAT - 7细胞的细胞体积。我们得出结论，非成釉细胞的牙上皮表达NKCC1以调节釉质器官中的细胞体积，并为成釉细胞提供将矿物质离子和碳酸氢根离子转运到釉质中所需的钠、钾和氯离子。功能性Nkcc1的缺失可能由其他类型的离子通道和离子转运蛋白补偿。在Nkcc1基因缺失小鼠的釉质器官细胞中连接蛋白43含量增加，表明这些细胞显示出更多的缝隙连接以增加细胞间通讯。
Na+:K+:2Cl− cotransporters (NKCCs) belong to the SLC12A family of cation-coupled Cl− transporters. We investigated whether enamel-producing mouse ameloblasts express NKCCs. Transcripts for Nkcc1 were identified in the mouse dental epithelium by RT-qPCR and NKCC1 protein was immunolocalized in outer enamel epithelium and in the papillary layer but not the ameloblast layer. In incisors of Nkcc1-null mice late maturation ameloblasts were disorganized, shorter and the mineral density of the enamel was reduced by 10% compared to wild-type controls. Protein levels of gap junction protein connexin 43, Na+-dependent bicarbonate cotransporter e1 (NBCe1), and the Cl−-dependent bicarbonate exchangers SLC26A3 and SLC26A6 were upregulated in Nkcc1-null enamel organs while the level of NCKX4/SLC24A4, the major K+, Na+ dependent Ca2+ transporter in maturation ameloblasts, was slightly downregulated. Whole-cell voltage clamp studies on rat ameloblast-like HAT-7 cells indicated that bumetanide increased ion-channel activity conducting outward currents. Bumetanide also reduced cell volume of HAT-7 cells. We concluded that non-ameloblast dental epithelium expresses NKCC1 to regulate cell volume in enamel organ and provide ameloblasts with Na+, K+ and Cl− ions required for the transport of mineral- and bicarbonate-ions into enamel. Absence of functional Nkcc1 likely is compensated by other types of ion channels and ion transporters. The increased amount of Cx43 in enamel organ cells in Nkcc1-null mice suggests that these cells display a higher number of gap junctions to increase intercellular communication.
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影响因子：
7.6
作者：
Lyaruu, D. M.;Medina, J. F.;Bronckers, A. L. J. J.
通讯作者：
Bronckers, A. L. J. J.
影响因子：
5.6
作者：
Lacruz, Rodrigo S.;Smith, Charles E.;Moffatt, Pierre;Chang, Eugene H.;Bromage, Timothy G.;Bringas, Pablo, Jr.;Nanci, Antonio;Baniwal, Sanjeev K.;Zabner, Joseph;Welsh, Michael J.;Kurtz, Ira;Paine, Michael L.
通讯作者：
Paine, Michael L.
影响因子：
4.2
作者：
Lacruz, Rodrigo S.;Nanci, Antonio;Kurtz, Ira;Wright, J. Timothy;Paine, Michael L.
通讯作者：
Paine, Michael L.
影响因子：
3.4
作者：
Gagnon, F;Orlov, SN;Hamet, P
通讯作者：
Hamet, P
影响因子：
7.6
作者：
Jalali, R.;Zandieh-Doulabi, B.;Bronckers, A. L. J. J.
通讯作者：
Bronckers, A. L. J. J.