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Editorial
. 2016 Aug 19;119(5):574-6.
doi: 10.1161/CIRCRESAHA.116.309442.

Plasticity of Arterial and Venous Endothelial Cell Identity: Some Nerve!

Basak Icli  1 , Mark W Feinberg  2
Affiliations
Editorial

Plasticity of Arterial and Venous Endothelial Cell Identity: Some Nerve!

Basak Icli et al. Circ Res. .
No abstract available

Keywords: Editorials; arteries; endothelial cells; pulmonary embolism; thrombosis; veins.

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Figures

Figure
Figure. Sympathetic nerve activation of α-adrenergic signaling regulates endothelial cell plasticity
Norepinephrine, a catecholamine synthesized and released by the sympathetic nervous system, binds and activates α1 and α2 adrenergic receptors (α1R and α2R) on target cells. This process results in the recruitment of the G proteins Gq and Gi and subsequent downstream activation of phospholipase-C (PLC) by α1R or inhibition of adenylate cyclase/protein kinase A (PKA) signaling pathways by α2R, effects that both promote ERK activation. α1R- and α2R-mediated activation of ERK induces arterial gene programming, in part, through increasing the expression of EfnB2, Dll4, Nrp1 and negatively regulating the expression of venous-associated genes EphB4, CoupTFII, and Apj. VEGF-mediated ERK activation is also known to positively regulate arterial endothelial cell fate, although how sympathetic innervation interacts with this pathway is not clear.
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