Altered β-adrenergic response in mice lacking myotonic dystrophy protein kinase

Muscle Nerve. 2012 Jan;45(1):128-30. doi: 10.1002/mus.22256.

Abstract

The protein kinase product of the gene mutated in myotonic dystrophy 1 (DMPK) is reported to play a role in cardiac pathophysiology. To gain insight into the molecular mechanisms modulated by DMPK, we characterize the impact of DMPK ablation in the context of cardiac β-adrenergic function. Our data demonstrate that DMPK knockout mice present altered β-agonist-induced responses and suggest that this is due, at least in part, to a reduced density of β(1)-adrenergic receptors in cardiac plasma membranes.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adrenergic beta-Agonists / pharmacology
  • Animals
  • Cell Membrane / drug effects
  • Disease Models, Animal
  • Dose-Response Relationship, Drug
  • Echocardiography
  • Isoproterenol / pharmacology
  • Mice
  • Mice, Knockout
  • Myocardium / cytology
  • Myotonic Dystrophy / genetics
  • Myotonic Dystrophy / pathology
  • Myotonic Dystrophy / physiopathology
  • Myotonin-Protein Kinase
  • Phosphorylation / drug effects
  • Protein Serine-Threonine Kinases / deficiency*
  • Receptors, Adrenergic, beta / blood
  • Receptors, Adrenergic, beta / metabolism*
  • Serine / metabolism
  • Sodium-Potassium-Exchanging ATPase / metabolism
  • Vesicular Transport Proteins / metabolism

Substances

  • Adrenergic beta-Agonists
  • DMPK protein, mouse
  • Receptors, Adrenergic, beta
  • Vesicular Transport Proteins
  • early endosome antigen 1
  • Serine
  • Myotonin-Protein Kinase
  • Protein Serine-Threonine Kinases
  • Sodium-Potassium-Exchanging ATPase
  • Isoproterenol