The myoendothelial junction: connections that deliver the message

Abstract

A vast amount of investigation has centered on how the endothelium and smooth muscle communicate. From this evidence, myoendothelial junctions have emerged as critical anatomical structures to regulate heterocellular cross talk. Indeed, there is now evidence that the myoendothelial junction serves as a signaling microdomain to organize proteins used to facilitate vascular heterocellular communication. This review highlights the evolving role of myoendothelial junctions in the context of vascular cell-cell communication.

FIGURE 1.

Ultrastructure of the MEJ An electron micrograph of an MEJ from a spinotrapezeous muscle arteriole. Arrows point to organelles localized to the MEJ, including endoplasmic reticulum, ribosomes, and caveolae. Original image is from Ref. and used here with permission. Scale bar is 0.25 μm.

FIGURE 2.

Possible mechanism of NO control at the MEJ Hemoglobin α (Hbα) is synthesized by vascular ECs and is enriched at the MEJ, where it forms a complex with eNOS and the reductase CytB5R3. The NO generated by eNOS at the MEJ is able to diffuse to the overlying smooth muscle cell layer when Hbα resides in the Fe³⁺ state. Reduction of Hbα to the Fe²⁺ state by the activity of CytB5R3 promotes NO scavenging by Hbα, preventing NO diffusion. Presumably, the scavenging of NO by Hga in resistance arteries allows EDHF to predominate.