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Activation of TRPV4 channel in pancreatic INS‐1E beta cells enhances glucose‐stimulated insulin secretion via calcium‐dependent mechanisms
Author(s) -
Skrzypski M.,
Kakkassery M.,
Mergler S.,
Grötzinger C.,
Khajavi N.,
Sassek M.,
Szczepankiewicz D.,
Wiedenmann B.,
Nowak K.W.,
Strowski M.Z.
Publication year - 2013
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2013.08.025
Subject(s) - trpv4 , transient receptor potential channel , trpv , secretion , endocrinology , medicine , chemistry , ruthenium red , intracellular , insulin , calcium in biology , calcium , calcium channel , pancreatic islets , trpv1 , microbiology and biotechnology , receptor , biochemistry , biology , islet
Transient receptor potential channel vanilloid type 4 (TRPV4) is a Ca 2+ ‐ and Mg 2+ ‐permeable cation channel that influences oxidative metabolism and insulin sensitivity. The role of TRPV4 in pancreatic beta cells is largely unknown. Here, we characterize the role of TRPV4 in controlling intracellular Ca 2+ and insulin secretion in INS‐1E beta cells. Osmotic, thermal or pharmacological activation of TRPV4 caused a rapid rise of intracellular Ca 2+ and enhanced glucose‐stimulated insulin secretion. In the presence of the TRPV channel blocker ruthenium red (RuR) or after suppression of TRPV4 protein production, TRPV4 activators failed to increase [Ca 2+ ] i and insulin secretion in INS‐1E cells.