BH4-Mediated Enhancement of Endothelial Nitric Oxide Synthase Activity Reduces Hyperoxia-Induced Endothelial Damage and Preserves Vascular Integrity in the Neonate | Zendy

Kevin Edgar | Zendy; Orla Galvin | Zendy; Anthony Collins | Zendy; Zvonimir S. Katušić | Zendy; Denise McDonald | Zendy

Open Access

BH4-Mediated Enhancement of Endothelial Nitric Oxide Synthase Activity Reduces Hyperoxia-Induced Endothelial Damage and Preserves Vascular Integrity in the Neonate

Author(s) -

Kevin Edgar,

Orla Galvin,

Anthony Collins,

Zvonimir S. Katušić,

Denise McDonald

Publication year - 2017

Publication title -

investigative ophthalmology and visual science

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.935

H-Index - 218

eISSN - 1552-5783

pISSN - 0146-0404

DOI - 10.1167/iovs.16-20523

Subject(s) - hyperoxia , enos , citrulline , nitric oxide synthase , nitric oxide , nitrotyrosine , nitric oxide synthase type iii , endothelial nos , chemistry , endocrinology , biology , medicine , biochemistry , arginine , lung , amino acid

Endothelial nitric oxide synthase (eNOS)-derived nitric oxide (NO) has important vasoprotective functions that are compromised in the vasodegenerative phase of retinopathy of prematurity, owing to hyperoxia-induced depletion of the essential NOS cofactor BH4. Because modulating eNOS function can be beneficial or detrimental, our aim was to investigate the effect of BH4 supplementation on eNOS function and vascular regression in hyperoxia.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research