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Spinophilin is required for normal morphology, Ca(2+) homeostasis and contraction but dispensable for beta-adrenergic stimulation of adult cardiomyocytes

Item Type:Article
Title:Spinophilin is required for normal morphology, Ca(2+) homeostasis and contraction but dispensable for beta-adrenergic stimulation of adult cardiomyocytes
Creators Name:Petzhold, D. and da Costa-Goncalves, A.C. and Gross, V. and Morano, I.
Abstract:Spinophilin (SPN) is a ubiquitously expressed scaffolding protein that interacts through several binding modules with a variety of target proteins. Thus, SPN bundles F-actin, targets protein phosphatase 1 to the ryanodine receptor, and targets regulators of G-protein signaling to G-protein coupled receptors in cardiomyocytes. In this work we studied the role of SPN on cardiomyocyte morphology, function, and beta-adrenergic responsiveness using a homozygous SPN knock-out mouse model (SPN-/-). We show that spinophilin deficiency significantly (1) reduced cardiomyocyte length, (2) increases both Ca(2+) amplitude and maximal rate of Ca(2+) rise during systole, and (3) decreased shortening amplitude and maximal rate of shortening, while (4) beta-adrenergic stimulation remained intact. Our data suggest that spinophilin is an upstream regulator required for normal growth and excitation-contraction coupling, but is dispensable for beta-adrenergic stimulation of adult cardiomyocytes.
Keywords:Spinophilin, Scaffolding protein, Ca(2+) homeostasis, Contractility, Cardiomyocytes, Animals, Mice
Source:Journal of Muscle Research and Cell Motility
ISSN:0142-4319
Publisher:Springer (The Netherlands)
Volume:32
Number:4-5
Page Range:243-248
Date:December 2011
Official Publication:https://doi.org/10.1007/s10974-011-9259-4
PubMed:View item in PubMed

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