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Departments of 1 Physiology and Biophysics, 2 Cell Biology, and 4 Nephrology, University of Alabama at Birmingham, Birmingham, Alabama 35294; 3 Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas 66160; and 5 Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205
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 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+
concentration and secretory Cl
transport show 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.
polycystic kidney disease; adenosine 5'-triphosphate; autocrine; epithelia; purinergic receptors
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