Key result
DMPK knockout mice present altered β-agonist-induced responses, likely due to a reduced density of β(1)-adrenergic receptors in cardiac plasma membranes.
DMPK ablation alters cardiac β-adrenergic function by reducing β(1)-adrenergic receptor density, providing insight into cardiac pathophysiology in myotonic dystrophy 1.
Suggests DMPK involvement in myotonic dystrophy cardiac pathology; hypothesis-generating and should not yet change practice.
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.
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Llagostera et al. (2011) studied Myotonic dystrophy 1. DMPK ablation (knockout) was evaluated on β-agonist-induced responses and density of β(1)-adrenergic receptors. DMPK knockout mice present altered β-agonist-induced responses, likely due to a reduced density of β(1)-adrenergic receptors in cardiac plasma membranes.
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