
Rosiglitazone Promotes AQP2 Plasma Membrane Expression In Renal Cells Via a Ca2+-Dependent/cAMP-Independent Mechanism
Author(s) -
Giuseppe Procino,
Andrea Gerbino,
Serena Milano,
Maria Celeste Nicoletti,
Lisa Mastrofrancesco,
Monica Carmosino,
María Svelto
Publication year - 2015
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000373933
Subject(s) - aquaporin 2 , apical membrane , rosiglitazone , microbiology and biotechnology , endocrinology , aquaporin , intracellular , medicine , signal transduction , chemistry , kidney , cytosol , biology , receptor , membrane , biochemistry , mechanical engineering , water channel , engineering , inlet , enzyme
Thiazolidinediones are highly beneficial in the treatment of type II diabetes. However, they are also associated with edema and increased risk of congestive heart failure. Several studies demonstrated that rosiglitazone (RGZ) increases the abundance of aquaporin-2 (AQP2) at the plasma membrane of renal cells. The aim of this study was to investigate whether RGZ might activate a transduction pathway facilitating AQP2 membrane accumulation in renal cells.