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


  • D. Petzhold
  • A.C. da Costa-Goncalves
  • V. Gross
  • I. Morano


  • Journal of Muscle Research and Cell Motility


  • J Muscle Res Cell Motil 32 (4-5): 243-248


  • 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.