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PurposeHydrogen sulfide (H2S) is an endogenous gaseous signaling molecule with significant pathophysiological importance, but its role in retinal neovascular diseases is unknown. Hydrogen sulfide is generated from L-cysteine by cystathionine-β-synthase (CBS), cystathionine-γ-lyase (CSE), and/or 3-mercaptopyruvate sulfurtransferase (3-MST). The aim of this study was to investigate the role of H2S in retinal neovascularization (NV) in ischemia-induced retinopathy.MethodsStudies were performed in a murine model of oxygen-induced retinopathy (OIR). Hydrogen sulfide was detected with a fluorescent assay. Western blots and immunohistochemistry were used to assess the changes of H2S-producing enzymes. Gene deletion and pharmacologic inhibition were used to investigate the role of H2S in retinal NV.ResultsHydrogen sulfide production was markedly increased in retinas from OIR mice compared with those from room air (RA) controls. Cystathionine-β-synthase and CSE were significantly increased in OIR retinas, whereas 3-MST was not changed. Cystathionine-β-synthase was expressed throughout the neuronal retina and upregulated in neurons and glia during OIR. Cystathionine-γ-lyase was also localized to multiple retinal layers. Its immunoreactivity was prominently increased in neovascular tufts in OIR. Pharmacologic inhibition of CBS/CSE or genetic deletion of CSE significantly reduced retinal NV in OIR.ConclusionsOur data indicate that the H2S-generating enzymes/H2S contributes to retinal NV in ischemia-induced retinopathy and suggest that blocking this pathway may provide novel therapeutic approaches for the treatment of proliferative retinopathy.

Intracranial dural arteriovenous fistulas (dAVFs) can produce a variety of symptoms depending on fistula location, size, and venous drainage. Although cavernous sinus fistulas (CCFs) classically present with symptoms of orbital venous congestion due to retrograde venous drainage into the superior ophthalmic vein (i.e. an arterialised ''red eye'') (Miller NR. Neurosurg Focus 2007;23:1-15), dAVFs not localised to the cavernous sinus rarely present with a ''red eye'' and instead produce increased intracranial pressure, which can mimic idiopathic intracranial hypertension (IIH). The authors present a unique case of an intracranial dAVF with clinical features suggestive of both CCF and IIH. Clinicians should be aware of this possibility to avoid delayed diagnosis of the intracranial dAVF.

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