Escorting α-globin to eNOS: α-globin–stabilizing protein paves the way
Adam C. Straub, Mark T. Gladwin
Adam C. Straub, Mark T. Gladwin
Published November 1, 2018; First published October 8, 2018
Citation Information: J Clin Invest. 2018;128(11):4755-4757. https://doi.org/10.1172/JCI124302.
View: Text | PDF
Category: Commentary

Escorting α-globin to eNOS: α-globin–stabilizing protein paves the way

Abstract

In the vascular wall, endothelial nitric oxide synthase (eNOS) produces NO to regulate peripheral vascular resistance, tissue perfusion, and blood pressure. In resistance arteries, eNOS couples with α-globin and, through chemical reactions, modulates NO diffusion needed for vascular smooth muscle relaxation. While α-globin protein alone is known to be unstable, the mechanisms that enable α-globin protein expression remain elusive. Here, Lechauve et al. report that arterial endothelium expresses α hemoglobin–stabilizing protein, which acts as a critical chaperone protein for α-globin expression and vascular function.

Authors

Adam C. Straub, Mark T. Gladwin

×

Figure 1

Role of AHSP in the regulation of NO.

Options: View larger image (or click on image) Download as PowerPoint
Role of AHSP in the regulation of NO. (A) In resistance arteries and art...
(A) In resistance arteries and arterioles, a complex between α-globin, eNOS, and AHSP forms to stabilize and regulate NO diffusion from endothelium to smooth muscle to control vascular tone. (B) Loss of AHSP causes a decrease in α-globin expression, resulting in a concomitant increase in NO diffusion.