Blazer-Yost Bonnie L, Blacklock Brenda J, Flaig Stephanie, Bacallao Robert L, Gattone Vincent H
Department of Biology, Indiana University Purdue University Indianapolis, Indianapolis, IN 46202, USA.
Cell Physiol Biochem. 2011;28(6):1255-64. doi: 10.1159/000335857. Epub 2011 Dec 16.
Autosomal dominant polycystic kidney disease (ADPKD) is characterized by the slow growth of multiple fluid-filled cysts predominately in the kidney tubules and liver bile ducts. Elucidation of mechanisms that control cyst growth will provide the basis for rational therapeutic intervention. We used electrophysiological methods to identify lysophosphatidic acid (LPA) as a component of cyst fluid and serum that stimulates secretory Cl- transport in the epithelial cell type that lines renal cysts. LPA effects are manifested through receptors located on the basolateral membrane of the epithelial cells resulting in stimulation of channel activity in the apical membrane. Concentrations of LPA measured in human ADPKD cyst fluid and in normal serum are sufficient to maximally stimulate ion transport. Thus, cyst fluid seepage and/or leakage of vascular LPA into the interstitial space are capable of stimulating epithelial cell secretion resulting in cyst enlargement. These observations are particularly relevant to the rapid decline in renal function in late-stage disease and to the "third hit" hypothesis that renal injury exacerbates cyst growth.
常染色体显性多囊肾病(ADPKD)的特征是多个充满液体的囊肿主要在肾小管和肝胆管中缓慢生长。阐明控制囊肿生长的机制将为合理的治疗干预提供依据。我们使用电生理方法确定溶血磷脂酸(LPA)是囊肿液和血清的一种成分,它能刺激构成肾囊肿内衬的上皮细胞类型中的分泌性氯离子转运。LPA的作用通过位于上皮细胞基底外侧膜上的受体表现出来,从而刺激顶端膜中的通道活性。在人类ADPKD囊肿液和正常血清中测得的LPA浓度足以最大程度地刺激离子转运。因此,囊肿液渗漏和/或血管LPA漏入间质空间能够刺激上皮细胞分泌,导致囊肿增大。这些观察结果与疾病晚期肾功能的快速下降以及肾损伤加剧囊肿生长的“第三次打击”假说特别相关。