Ampawong S, Klincomhum A, Likitsuntonwong W, Singha O, Ketjareon T, Panavechkijkul Y, Zaw K M, Kengkoom K
Veterinary Medical Care Office, National Laboratory Animal Center, Mahidol University, Thailand.
J Comp Pathol. 2012 May;146(4):332-7. doi: 10.1016/j.jcpa.2011.08.005. Epub 2011 Sep 25.
This study investigates the expression of aquaporin-1, -2 and -4 in mice with a spontaneously-arising mutation that leads to hydronephrosis (ICR/Mlac-hydro mice). The mutant mice developed bilateral non-obstructive hydronephrosis without evidence of interstitial fibrosis or glomerulosclerosis. The mice had no abnormality in blood urea nitrogen or creatinine concentrations or in urine specific gravity. Despite the severity of the renal damage the mice grew and reproduced normally. Kidneys from the mutant mice had reduced expression of all three aquaporins compared with wild type mice. The reduction in aquaporin was proportional to the degree of hydronephrosis, but this change did not appear to be associated with disturbance of urinary function.
本研究调查了水通道蛋白-1、-2和-4在因自发突变导致肾积水的小鼠（ICR/Mlac-hydro小鼠）中的表达情况。突变小鼠出现双侧非梗阻性肾积水，无间质纤维化或肾小球硬化迹象。这些小鼠的血尿素氮、肌酐浓度及尿比重均无异常。尽管肾脏损伤严重，但小鼠生长和繁殖正常。与野生型小鼠相比，突变小鼠肾脏中所有三种水通道蛋白的表达均降低。水通道蛋白的减少与肾积水程度成正比，但这种变化似乎与尿功能紊乱无关。
