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Articles in PresS, published online ahead of print August 8, 2001
Am J Physiol Renal Physiol, 10.1152/ajprenal.0337.2000
Submitted on December 13, 2000
Accepted on June 26, 2001
1 Physiology and Biophysics, University of Alabama at Birmingham, Birmingham, AL, USA; Cell Biology, University of Alabama at Birmingham, Birmingham, AL, USA
2 Kidney Institute, University of Kansas Medical Center, Kansas City, KS, USA
3 Physiology and Biophysics, University of Alabama at Birmingham, Birmingham, AL, USA
4 Nephrology, University of Alabama at Birmingham, Birmingham, AL, USA
5 Physiology, Johns Hopkins University School of Medicine, Baltimore, MD, USA
6 Nephrology, University of Alabama at Birmingham, Birmingham, AL, USA; Cell Biology, University of Alabama at Birmingham, Birmingham, AL, USA
7 Nephrology, University of Alabama at Birmingham, Birmingham, AL, USA; Physiology and Biophysics, University of Alabama at Birmingham, Birmingham, AL, USA
* To whom correspondence should be addressed. E-mail: eschwiebert{at}physiology.uab.edu.
ATP and its metabolites are potent autocrine agonists that act extracellularly within tissues to affect epithelial function. In polycystic kidneys, renal tubules become dilated and/or encapsulated as cysts, creating abnormal microenvironments for autocrine signaling. Previously, our laboratory has shown that high nanomolar to micromolar quantities of ATP are released from cell monolayers in vitro and detectable in cyst fluids from microdissected human autosomal dominant polycystic kidney (ADPKD) cysts. Here, we show enhanced ATP release and ATP release dysregulation from autosomal recessive polycystic kidney (ARPKD) and ADPKD epithelial cell models. RT-PCR and immunoblotting for P2Y G protein-coupled receptors and P2X purinergic receptor channels show expression of mRNA and/or protein for multiple subtypes from both families. Assays of cytosolic Ca2+ and secretory Cl- transport shows P2Y and P2X purinergic receptor-mediated stimulation of Cl- secretion via cytosolic Ca2+-dependent signaling. Therefore, we hypothesize that autocrine purinergic signaling may augment detrimentally cyst volume expansion in ADPKD or tubule dilation in ARPKD, accelerating disease progression. Keywords: Polycystic Kidney Disease, ATP, Autocrine, Epithelia, Purinergic Receptors
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