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Title: ATP and PIP2 dependence of the magnesium-inhibited, TRPM7-like cation channel in cardiac myocytes
Authors: Gwanyanya, Asfree ×
Sipido, Karin
Vereecke, Johan
Mubagwa, Kanigula #
Issue Date: Sep-2006
Series Title: American Journal of Physiology. Cell Physiology vol:291 issue:4 pages:C627-35
Abstract: The Mg(2+)-inhibited cation (MIC) current (I(MIC)) in cardiac myocytes biophysically resembles currents of heterologously expressed transient receptor potential (TRP) channels, particularly TRPM6 and TRPM7, known to be important in Mg(2+) homeostasis. To understand the regulation of MIC channels in cardiac cells, we used the whole cell voltage-clamp technique to investigate the role of intracellular ATP in pig, rat, and guinea pig isolated ventricular myocytes. I(MIC), studied in the presence or absence of extracellular divalent cations, was sustained for >or=50 min after patch rupture in ATP-dialyzed cells, whereas in ATP-depleted cells I(MIC) exhibited complete rundown. Equimolar substitution of internal ATP by its nonhydrolyzable analog adenosine 5'-(beta,gamma-imido)triphosphate failed to prevent rundown. In ATP-depleted cells, inhibition of lipid phosphatases by fluoride + vanadate + pyrophosphate prevented I(MIC) rundown. In contrast, under similar conditions neither the inhibition of protein phosphatases 1, 2A, 2B or of protein tyrosine phosphatase nor the activation of protein kinase A (forskolin, 20 microM) or protein kinase C (phorbol myristate acetate, 100 nM) could prevent rundown. In ATP-loaded cells, depletion of phosphatidylinositol 4,5-bisphosphate (PIP(2)) by prevention of its resynthesis (10 microM wortmannin or 15 microM phenylarsine oxide) induced rundown of I(MIC). Finally, loading ATP-depleted cells with exogenous PIP(2) (10 microM) prevented rundown. These results suggest that PIP(2), likely generated by ATP-utilizing lipid kinases, is necessary for maintaining cardiac MIC channel activity.
URI: 
ISSN: 0363-6143
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Experimental Cardiac Surgery
Cardiology
Laboratory of Molecular and Cellular Signaling
Experimental Cardiology
Department of Cellular and Molecular Medicine - miscellaneous
× corresponding author
# (joint) last author

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