Sands J M
Renal Division, Department of Medicine and Department of Physiology, Emory University School of Medicine, 1639 Pierce Dr., NE, Atlanta, GA 30322, USA.
J Membr Biol. 2003 Feb 1;191(3):149-63. doi: 10.1007/s00232-002-1053-1.
Physiologic data provided evidence for specific urea transporter proteins in red blood cells and kidney inner medulla. During the past decade, molecular approaches resulted in the cloning of several urea transporter cDNA isoforms derived from two gene families: UT-A and UT-B. Polyclonal antibodies were generated to the cloned urea transporter proteins, and their use in integrative animal studies resulted in several novel findings, including: (1) UT-B is the Kidd blood group antigen; (2) UT-B is also expressed in many non-renal tissues and endothelial cells; (3) vasopressin increases UT-A1 phosphorylation in rat inner medullary collecting duct; (4) the surprising finding that UT-A1 protein abundance and urea transport are increased in the inner medulla during conditions in which urine concentrating ability is reduced; and (5) UT-A protein abundance is increased in uremia in both liver and heart. This review will summarize the knowledge gained from studying molecular mechanisms of urea transport and from integrative studies into urea transporter protein regulation.
生理学数据为红细胞和肾内髓中的特定尿素转运蛋白提供了证据。在过去十年中,分子生物学方法使得从两个基因家族(UT-A和UT-B)克隆出了几种尿素转运体cDNA亚型。针对克隆出的尿素转运蛋白制备了多克隆抗体,将其用于整体动物研究产生了几个新发现,包括:(1)UT-B是基德血型抗原;(2)UT-B也在许多非肾组织和内皮细胞中表达;(3)血管加压素可增加大鼠内髓集合管中UT-A1的磷酸化;(4)一个惊人的发现是,在尿浓缩能力降低的情况下,内髓中的UT-A1蛋白丰度和尿素转运增加;以及(5)尿毒症时肝脏和心脏中的UT-A蛋白丰度增加。本综述将总结从研究尿素转运分子机制以及尿素转运蛋白调节的整体研究中获得的知识。