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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 October 8, 2018
Citation Information: J Clin Invest. 2018;128(11):4755-4757. https://doi.org/10.1172/JCI124302.
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Commentary Article has an altmetric score of 5

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

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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

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Figure 1

Role of AHSP in the regulation of NO.

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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.

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ISSN: 0021-9738 (print), 1558-8238 (online)

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