BDNF Actions in the Cardiovascular System: Roles in Development, Adulthood and Response to Injury

Abstract

The actions of BDNF (Brain-derived Neurotrophic Factor) in regulating neuronal development and modulating synaptic activity have been extensively studied and well established. Equally important roles for this growth factor have been uncovered in the cardiovascular system, through the examination of gene targeted animals to define critical actions in development, and to the unexpected roles of BDNF in modulating the response of the heart and vasculature to injury. Here we review the compartmentally distinct realm of cardiac myocytes, vascular smooth muscle cells, endothelial cells, and hematopoietic cells, focusing upon the actions of BDNF to modulate contractility, migration, neoangiogenesis, apoptosis and survival. These studies indicate that BDNF is an important growth factor which directs the response of the cardiovascular system to acute and chronic injury.

Keywords: BDNF; TrkB; cardiovascular system; myocardial infarction; myocyte; vascular injury.

FIGURE 1

Section of adult human myocardium, stained with hematoxylin and eosin and annotated with expression of neurotrophins and neurotrophin receptors in the indicated cell types. Data was derived from Scarisbrick et al. (1993); Yamamoto et al. (1996), Donovan et al. (2000); Wagner et al. (2005), Anastasia et al. (2014), and Fulgenzi et al. (2015).

FIGURE 2

Section of adult human iliac artery, stained with hematoxylin and eosin and annotated with expression of neurotrophins and their receptors in the indicated cell types. Data was derived from Scarisbrick et al. (1993); Donovan et al. (1995), Yamamoto et al. (1996); Kramer (2002), Kraemer et al. (2005), and Chacó-Fernández et al. (2016).

FIGURE 3

Section of adult human myocardium following myocardial infarction, in the border zone. Section was stained with hematoxylin and eosin and annotated with expression of neurotrophins and neurotrophin receptors. Data was derived from Kermani et al. (2005), Liu et al. (2006), Cai et al. (2006), Okada et al. (2010), Cao et al. (2012), Siao et al. (2012), and Halade et al. (2013).