Skip to main content
eScholarship
Open Access Publications from the University of California

Constitutive BDNF/TrkB signaling is required for normal cardiac contraction and relaxation.

  • Author(s): Feng, Ning
  • Huke, Sabine
  • Zhu, Guangshuo
  • Tocchetti, Carlo G
  • Shi, Sa
  • Aiba, Takeshi
  • Kaludercic, Nina
  • Hoover, Donald B
  • Beck, Sarah E
  • Mankowski, Joseph L
  • Tomaselli, Gordon F
  • Bers, Donald M
  • Kass, David A
  • Paolocci, Nazareno
  • et al.

Published Web Location

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4330748/
No data is associated with this publication.
Abstract

BDNF and its associated tropomyosin-related kinase receptor B (TrkB) nurture vessels and nerves serving the heart. However, the direct effect of BDNF/TrkB signaling on the myocardium is poorly understood. Here we report that cardiac-specific TrkB knockout mice (TrkB(-/-)) display impaired cardiac contraction and relaxation, showing that BDNF/TrkB signaling acts constitutively to sustain in vivo myocardial performance. BDNF enhances normal cardiomyocyte Ca(2+) cycling, contractility, and relaxation via Ca(2+)/calmodulin-dependent protein kinase II (CaMKII). Conversely, failing myocytes, which have increased truncated TrkB lacking tyrosine kinase activity and chronically activated CaMKII, are insensitive to BDNF. Thus, BDNF/TrkB signaling represents a previously unidentified pathway by which the peripheral nervous system directly and tonically influences myocardial function in parallel with β-adrenergic control. Deficits in this system are likely additional contributors to acute and chronic cardiac dysfunction.

Many UC-authored scholarly publications are freely available on this site because of the UC's open access policies. Let us know how this access is important for you.

Item not freely available? Link broken?
Report a problem accessing this item