Price Karen L, Sautin Yuri Y, Long David A, Zhang Li, Miyazaki Hiroki, Mu Wei, Endou Hitoshi, Johnson Richard J
Division of Nephrology, Hypertension, and Transplantation, University of Florida, Gainesville, Florida, USA.
J Am Soc Nephrol. 2006 Jul;17(7):1791-5. doi: 10.1681/ASN.2006030264. Epub 2006 Jun 14.
An elevated serum uric acid is associated with the development of hypertension and renal disease. Renal regulation of urate excretion is largely controlled by URAT1 (SLC22A12), a member of the organic anion transporter superfamily. This study reports the specific expression of URAT1 on human aortic vascular smooth muscle cells, as assessed by reverse transcription-PCR and Western blot analysis. Expression of URAT1 was localized to the cell membrane. Evidence that the URAT1 transporter was functional was provided by the finding that uptake of 14C-urate was significantly inhibited in the presence of probenecid, an organic anion transporter inhibitor. It is proposed that URAT1 may provide a mechanism by which uric acid enters the human vascular smooth muscle cell, a finding that may be relevant to the role of uric acid in cardiovascular disease.
血清尿酸升高与高血压和肾脏疾病的发生有关。尿酸排泄的肾脏调节主要由URAT1（SLC22A12）控制，它是有机阴离子转运体超家族的一员。本研究通过逆转录-聚合酶链反应和蛋白质印迹分析评估了URAT1在人主动脉血管平滑肌细胞上的特异性表达。URAT1的表达定位于细胞膜。有机阴离子转运体抑制剂丙磺舒存在时，14C-尿酸的摄取显著受到抑制，这一发现证明了URAT1转运体具有功能。有人提出，URAT1可能提供了一种尿酸进入人血管平滑肌细胞的机制，这一发现可能与尿酸在心血管疾病中的作用有关。
