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首页> 外文期刊>American Journal of Physiology >Ammonium transport in the colonic crypt cell line, T84: role for Rhesus glycoproteins and NKCC1
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Ammonium transport in the colonic crypt cell line, T84: role for Rhesus glycoproteins and NKCC1

机译：结肠隐窝细胞系中的铵转运，T84：恒河猴糖蛋白和NKCC1的作用

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First published November 21, 2007; doi: 10.1152/ajpgi.00251.2006.-Although colonic lumen NH levels are high, 15-44 mM normal range in humans, relatively few studies have addressed the transport mechanisms for NH4~+. More extensive studies have elucidated the transport of NH_4~+ in the kidney collecting duct, which involves a number of transporter processes also present in the distal colon. Similar to NH4~+ secretion in the renal collecting duct, we show that the distal colon secretory model, T84 cell line, has the capacity to secrete NH4~+ and maintain an apical-to-basolateral NH~+ gradient. NH4~+ transport in the secretory direction was supported by basolateral NH4~+ loading on NKCC1, Na+-K+-ATPase, and the NH~+ transporter, RhBG. NH4~++ was transported on NKCC1 in T84 cells nearly as well as K+ as determined by bumetanide-sensitive 86Rb-uptake. 86Rb-uptake and ouabain-sensitive current measurement indicated that NH4~+ is transported by Na+-K+-ATPase in these cells to an equal extent as K+. T84 cells expressed mRNA for the basolateral NH4+ transporter RhBG and the apical NH4~+ transporter RhCG. Net NH4~+ transport in the secretory direction determined by 14C-methylammonium (MA) uptake and flux occurred in T84 cells suggesting functional RhG protein activity. The occurrence of NH4~+ transport in the secretory direction within a colonic crypt cell model likely serves to minimize net absorption of NH4~+ because of surface cell NH4~+ absorption. These findings suggest that we rethink the present limited understanding of NH4~+ handling by the distal colon as being due solely to passive absorption.
机译：2007年11月21日第一次出版; DOI：10.1152 / AJPGI.00251.2006.尽管结肠腔NH水平高，人类的正常范围为15-44毫米，研究相对较少地解决了NH4〜+的运输机制。更广泛的研究阐明了肾脏收集管道中NH_4〜+的运输，这涉及许多还存在于远端结肠中的转运蛋白过程。与肾脏收集管道中的NH4〜+分泌物类似，我们表明远端结肠分泌模型T84细胞系具有分泌NH4〜+的能力，并维持到基于基底外侧NH〜+梯度。 NH4〜+在分泌方向上的运输是通过基底间NH4〜+负载的NKCC1，Na + -K + -ATP酶和NH〜+ Transporter，RHBG支持。 NH4〜++几乎在T84细胞中在NKCC1上运输，并且通过胆敏敏感的86RB-uptake测定。 86RB-摄取和Oubabain敏感电流测量表明NH4〜+在这些细胞中的Na + -k + -AtPase在这些细胞中运输至相等程度为K +。 T84细胞表达了基石外侧NH4 +转运蛋白RHBG和顶端NH4〜+转运蛋白的mRNA。在T84细胞中由14℃-甲基铵（MA）摄取和助焊剂测定的分泌方向上的净NH4〜+传输在提出官能性RHG蛋白质活性。在结肠隐窝细胞模型中的分泌方向上的NH4〜+传输的发生可能是因为由于表面细胞NH4〜+吸收，最小化NH4〜+的净吸收。这些研究结果表明，我们重新思考对NH4〜+处理的目前的有限理解，远端结肠作为被动吸收所造成的。

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