Constitutive BDNF/TrkB signaling is required for normal cardiac contraction and relaxation
Copyright policy )Constitutive BDNF/TrkB signaling is required for normal cardiac contraction and relaxation
Significance BDNF plays a key role in neuron development, survival, and function, with actions occurring through the stimulation of the tropomyosin-related kinase receptor B (TrkB) receptor. Whether BDNF/TrkB signaling has any physiologic role in governing myocardial function is unknown. Here we report that intact BDNF/TrkB signaling is required for the heart to fully contract and relax. These actions occur independently from and in addition to β-adrenergic influence. BDNF-induced enhancement of myocardial performance occurs via direct modulation of Ca 2+ cycling in a calmodulin-dependent protein kinase II-dependent manner. Thus, BDNF/TrkB signaling represents a previously unidentified way by which the peripheral nervous system controls cardiac muscle physiology. Our study suggests that loss or alterations in BDNF/TrkB stimulation may contribute to the pathogenesis of myocardial dysfunction in acute or chronic disease conditions.
- Vanderbilt University United States
- Johns Hopkins University United States
- East Tennessee State University United States
- University of Perugia Italy
- National Cerebral and Cardiovascular Center Japan
Patch-Clamp Techniques, Knockout, TrkB receptor, Medical Physiology, 610, Cardiovascular, neurotrophins, Mice, Diastole, 2.1 Biological and endogenous factors, Animals, Receptor, trkB, Calcium Signaling, Aetiology, Mice, Knockout, Analysis of Variance, CaMKII, Biomedical and Clinical Sciences, Brain-Derived Neurotrophic Factor, Neurosciences, Hemodynamics, Biomedical Sciences, Immunohistochemistry, Myocardial Contraction, Heart Disease, BDNF, trkB, cardiac contractility/relaxation, Calcium, Receptor
Patch-Clamp Techniques, Knockout, TrkB receptor, Medical Physiology, 610, Cardiovascular, neurotrophins, Mice, Diastole, 2.1 Biological and endogenous factors, Animals, Receptor, trkB, Calcium Signaling, Aetiology, Mice, Knockout, Analysis of Variance, CaMKII, Biomedical and Clinical Sciences, Brain-Derived Neurotrophic Factor, Neurosciences, Hemodynamics, Biomedical Sciences, Immunohistochemistry, Myocardial Contraction, Heart Disease, BDNF, trkB, cardiac contractility/relaxation, Calcium, Receptor
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