Molecular mechanisms regulating aquaporin-2 in kidney collecting duct
Author(s) -
Hyun Jun Jung,
TaeHwan Kwon
Publication year - 2016
Publication title -
american journal of physiology-renal physiology
Language(s) - English
Resource type - Journals
eISSN - 1931-857X
pISSN - 1522-1466
DOI - 10.1152/ajprenal.00485.2016
Subject(s) - aquaporin 2 , aquaporin , aquaporin 3 , apical membrane , vasopressin , microbiology and biotechnology , rhoa , reabsorption , kidney , homeostasis , chemistry , biology , endocrinology , signal transduction , biochemistry , water channel , membrane , mechanical engineering , inlet , engineering
The kidney collecting duct is an important renal tubular segment for regulation of body water homeostasis and urine concentration. Water reabsorption in the collecting duct principal cells is controlled by vasopressin, a peptide hormone that induces the osmotic water transport across the collecting duct epithelia through regulation of water channel proteins aquaporin-2 (AQP2) and aquaporin-3 (AQP3). In particular, vasopressin induces both intracellular translocation of AQP2-bearing vesicles to the apical plasma membrane and transcription of the Aqp2 gene to increase AQP2 protein abundance. The signaling pathways, including AQP2 phosphorylation, RhoA phosphorylation, intracellular calcium mobilization, and actin depolymerization, play a key role in the translocation of AQP2. This review summarizes recent data demonstrating the regulation of AQP2 as the underlying molecular mechanism for the homeostasis of water balance in the body.
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