Brain derived neurotrophic factor is an endothelial cell survival factor required for intramyocardial vessel stabilization.
Level 5 - mechanism / opinion, no new human data
Bench and animal research (knockout/transgenic mouse models and cell culture).
PubMed 11023857 · doi:10.1242/dev.127.21.4531
What was done
The authors evaluated the role of brain-derived neurotrophic factor (BDNF) and its receptor trkB in cardiac vascular development using BDNF-knockout (BDNF-/-) mice, transgenic mice with ectopic midgestational cardiac overexpression of BDNF, and primary cultures of neonatal mouse cardiac microvascular endothelial cells.
What was found
The abstract reports no numerical values. BDNF deficiency in mice caused loss of endothelial cell-cell contacts, increased endothelial apoptosis in intramyocardial arteries and capillaries, localized intraventricular wall hemorrhage, reduced cardiac contractility, and early postnatal death. Ectopic cardiac BDNF overexpression in midgestational mice increased capillary density. In cell culture, BDNF activation of endogenous trkB receptors promoted the survival of neonatal cardiac microvascular endothelial cells.
Why it matters
This work demonstrates a non-neuronal function for neurotrophins, establishing BDNF as an essential local factor for intramyocardial vascular stabilization and endothelial survival.
Limits
Findings are limited to murine genetic models and in vitro cell culture, with unverified applicability to human cardiac physiology. The abstract provides no quantitative data, sample sizes, or statistical metrics.
Cited by
- supports Homozygous knockout of the BDNF gene in mice is lethal.