Takakura Ayumi, Contrino Leah, Zhou Xiangzhi, Bonventre Joseph V, Sun Yanping, Humphreys Benjamin D, Zhou Jing
Renal Division, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, 4 Blackfan Circle, Boston, MA 02115, USA.
Hum Mol Genet. 2009 Jul 15;18(14):2523-31. doi: 10.1093/hmg/ddp147. Epub 2009 Apr 2.
The 'two-hit' model is a widely accepted genetic mechanism for progressive cyst formation in autosomal dominant polycystic kidney disease. We have previously shown that adult inactivation of Pkd1 using the Mx1Cre(+) allele causes a late onset of focal cystic disease. An explanation for the delayed appearance of cysts is the requirement for an additional independent factor, or 'third hit'. Here we show that renal injury leads to massive cystic disease in the same mouse line. Cysts are labeled with a collecting duct/tubule marker, Lectin Dolichos biflorus Agglutinin, which correlates with the site of Cre-mediated recombination in the collecting system. 5-Bromo-2'-deoxyuridine labeling reveals that cyst-lining epithelial cells are comprised of regenerated cells in response to renal injury. These data demonstrate, for the first time, a role for polycystin-1 in kidney injury and repair and indicate that renal injury constitutes a 'third hit' resulting in rapid cyst formation in adulthood.
“双打击”模型是常染色体显性多囊肾病中进行性囊肿形成的一种广泛接受的遗传机制。我们之前已经表明,使用Mx1Cre(+)等位基因在成年期使Pkd1失活会导致局灶性囊性疾病的迟发性发作。囊肿延迟出现的一种解释是需要一个额外的独立因素,即“第三次打击”。在此我们表明,肾损伤会在同一小鼠品系中导致大规模囊性疾病。囊肿用一种集合管/肾小管标记物——双花扁豆凝集素(Lectin Dolichos biflorus Agglutinin)标记,这与集合系统中Cre介导的重组位点相关。5-溴-2'-脱氧尿苷标记显示,囊肿衬里上皮细胞由响应肾损伤的再生细胞组成。这些数据首次证明了多囊蛋白-1在肾损伤和修复中的作用,并表明肾损伤构成“第三次打击”,导致成年期快速形成囊肿。