eNOS Overexpression Exacerbates Vascular Closure in the Obliterative Phase of OIR and Increases Angiogenic Drive in the Subsequent Proliferative Stage | Zendy

Kevin Edgar | Zendy; Tom A. Gardiner | Zendy; Rien van Haperen | Zendy; Rini de Crom | Zendy; Denise McDonald | Zendy

Open Access

eNOS Overexpression Exacerbates Vascular Closure in the Obliterative Phase of OIR and Increases Angiogenic Drive in the Subsequent Proliferative Stage

Author(s) -

Kevin Edgar,

Tom A. Gardiner,

Rien van Haperen,

Rini de Crom,

Denise McDonald

Publication year - 2012

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.12-9797

Subject(s) - enos , superoxide , hyperoxia , angiogenesis , endocrinology , nitric oxide , nitric oxide synthase type iii , medicine , neovascularization , vascular endothelial growth factor , nitric oxide synthase , nitrotyrosine , chemistry , biology , biochemistry , lung , vegf receptors , enzyme

In ischemic retinopathies, the misdirection of reparative angiogenesis away from the hypoxic retina leads to pathologic neovascularization. Thus, therapeutic strategies that reverse this trend would be extremely beneficial. Nitric oxide (NO) produced by endothelial nitric oxide synthase (eNOS) is an important mediator of vascular endothelial growth factor (VEGF) function facilitating vascular growth and maturation. However, in addition to NO, eNOS can also produce superoxide (O(2)(-)), exacerbating pathology. Here, our aim was to investigate the effect of eNOS overexpression on vascular closure and subsequent recovery of the ischemic retina.

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