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| 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., da Costa-Goncalves, A.C., 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 |
| 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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