Jaykumar Ankita Bachhawat, Caceres Paulo S, Sablaban Ibrahim, Tannous Bakhos A, Ortiz Pablo A
Hypertension and Vascular Research, Henry Ford Hospital, Detroit, Michigan; Department of Physiology, Wayne State University, Detroit, Michigan; and.
Hypertension and Vascular Research, Henry Ford Hospital, Detroit, Michigan;
Am J Physiol Renal Physiol. 2016 Jan 15;310(2):F183-91. doi: 10.1152/ajprenal.00104.2015. Epub 2015 Nov 4.
The apical Na-K-2Cl cotransporter (NKCC2) mediates NaCl reabsorption by the thick ascending limb (TAL). The amount of NKCC2 at the apical membrane of TAL cells is determined by exocytic delivery, recycling, and endocytosis. Surface biotinylation allows measurement of NKCC2 endocytosis, but it has low time resolution and does not allow imaging of the dynamic process of endocytosis. We hypothesized that total internal reflection fluorescence (TIRF) microscopy imaging of labeled NKCC2 would allow monitoring of NKCC2 endocytosis in polarized Madin-Darby canine kidney (MDCK) and TAL cells. Thus we generated a NKCC2 construct containing a biotin acceptor domain (BAD) sequence between the transmembrane domains 5 and 6. Once expressed in polarized MDCK or TAL cells, surface NKCC2 was specifically biotinylated by exogenous biotin ligase (BirA). We also demonstrate that expression of a secretory form of BirA in TAL cells induces metabolic biotinylation of NKCC2. Labeling biotinylated surface NKCC2 with fluorescent streptavidin showed that most apical NKCC2 was located within small discrete domains or clusters referred to as "puncta" on the TIRF field. NKCC2 puncta were observed to disappear from the TIRF field, indicating an endocytic event which led to a decrease in the number of surface puncta at a rate of 1.18 ± 0.16%/min in MDCK cells, and a rate 1.09 ± 0.08%/min in TAL cells (n = 5). Treating cells with a cholesterol-chelating agent (methyl-β-cyclodextrin) completely blocked NKCC2 endocytosis. We conclude that TIRF microscopy of labeled NKCC2 allows the dynamic imaging of individual endocytic events at the apical membrane of TAL cells.
顶端钠-钾-2氯协同转运蛋白(NKCC2)介导厚壁升支粗段(TAL)对氯化钠的重吸收。TAL细胞顶端膜上NKCC2的量由胞吐转运、循环利用和内吞作用决定。表面生物素化可用于测量NKCC2的内吞作用,但时间分辨率较低,且无法对内吞作用的动态过程进行成像。我们推测,对标记的NKCC2进行全内反射荧光(TIRF)显微镜成像,将能够监测极化的麦氏达比犬肾(MDCK)细胞和TAL细胞中NKCC2的内吞作用。因此,我们构建了一个NKCC2构建体,该构建体在跨膜结构域5和6之间包含一个生物素受体结构域(BAD)序列。一旦在极化的MDCK或TAL细胞中表达,表面的NKCC2就会被外源性生物素连接酶(BirA)特异性生物素化。我们还证明,在TAL细胞中表达分泌形式的BirA会诱导NKCC2的代谢性生物素化。用荧光链霉亲和素标记生物素化的表面NKCC2表明,大多数顶端NKCC2位于TIRF视野中称为“亮点”的小离散区域或簇内。观察到NKCC2亮点从TIRF视野中消失,这表明发生了内吞事件,导致表面亮点数量减少,在MDCK细胞中的减少速率为1.18±0.16%/分钟,在TAL细胞中的减少速率为1.09±0.08%/分钟(n = 5)。用胆固醇螯合剂(甲基-β-环糊精)处理细胞可完全阻断NKCC2的内吞作用。我们得出结论,对标记的NKCC2进行TIRF显微镜成像能够对TAL细胞顶端膜上的单个内吞事件进行动态成像。