NaHS induces relaxation response in prostaglandin F2α precontracted bovine retinal arteries partially via Kv and Kir channels

Takır, Selçuk; Ortaköylü, G.Z.; Toprak, Ayça; Uydeş-Doğan, B. Sönmez

doi:10.1016/j.exer.2015.02.002

Cited by 18 publications

(9 citation statements)

References 33 publications

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“… 22 , 23 The role of H 2 S in retinal pathophysiological changes has been appreciated in the past decade. Studies discovered several protective properties of H 2 S in a variety of conditions, including protecting retina from light-induced degeneration by suppression of Ca 2+ influx, 10 attenuating excitotoxic neurotransmission, 9 protecting retinal neuronal cell apoptosis against NMDA or retinal ischemia-reperfusion–induced injury via its antioxidative activity, 11 , 12 , 24 inducing retinal vascular relaxation, 25 , 26 and alleviating retinal oxidative stress and inflammation in a rat model of streptozotocin-induced diabetes. 27 In spite of this progress, the function of H 2 S in neovascular disease in the retina is unknown, although increased plasma and vitreous H 2 S has been found in patients with proliferative diabetic retinopathy, 28 and H 2 S exhibits proangiogenic property in organs where ischemic vessel growth is beneficial.…”

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confidence: 99%

Hydrogen Sulfide Contributes to Retinal Neovascularization in Ischemia-Induced Retinopathy

Gersztenkorn

Coletta

Zhu

et al. 2016

Invest. Ophthalmol. Vis. Sci.

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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.

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mentioning

confidence: 99%

Hydrogen Sulfide Contributes to Retinal Neovascularization in Ischemia-Induced Retinopathy

Gersztenkorn

Coletta

Zhu

et al. 2016

Invest. Ophthalmol. Vis. Sci.

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“…H 2 S is probably formed by CBS and not by CSE in bovine retina, because the relaxation induced by L-cysteine could be blocked by a CBS inhibitor but not by a CSE inhibitor. 33 This is in contrast to the findings on porcine retinal arterioles where the CBS and CSE blockers both could inhibit the vasorelaxing influence of L-cysteine. The effect of the CBS and CSE blockers was larger in the presence of retinal tissue and during hypoxia.…”

Section: Retinal Relaxing Factor and Hydrogen Sulfidementioning

confidence: 71%

“…32 The H 2 S donor GYY4137 is able to induce a substantial vasorelaxation in porcine retinal arterioles and the H 2 S donor NaHS in porcine and bovine retinal arteries. 18,33 The NaHS-induced relaxation is reduced in the presence of 100 mM K þ , just like the RRFinduced relaxation. Further research revealed that the H 2 S relaxation was endothelium, NO, COX, guanylyl cyclase, and adenylyl cyclase independent, but that K ir and K V channels are involved.…”

Section: Retinal Relaxing Factor and Hydrogen Sulfidementioning

confidence: 98%

The Retinal Relaxing Factor: Update on an Enigmatic Regulator of the Retinal Circulation

Daele

Boydens

Pauwels

et al. 2017

Invest. Ophthalmol. Vis. Sci.

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The retinal circulation is regulated by different local factors and might include the retinal relaxing factor (RRF). This factor is found to be continuously released by the retina and relaxes smooth muscle cells. This review describes the current knowledge about the RRF. Despite many research efforts, the cellular source, identity, mechanism, and physiological role of the RRF remain largely unknown. Thus far, it seems that the RRF is a hydrophilic, thermostable, diffusible chemical messenger, which characteristics do not correspond with most well-known endogenous vasorelaxants. The RRF-induced relaxation seems to rely on activation of the inward rectifier K+ channels and the Rho kinase Ca2+ sensitization mechanism. Voltage-dependent K+ channels and plasma membrane Ca2+-ATPase might also be involved, whereas the involvement of cyclooxygenase is still a point of discussion. Furthermore, it appears that the RRF is involved in other relaxation pathways, namely those of hypoxia, adenosine, and adenosine triphosphate, hydrogen sulfide, γ-aminobutyric acid, and dorzolamide.

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“…Njie-Mbye et al found that glibenclamide, a K ATP channel inhibitor, inhibited the H 2 S donor NaHS-induced cyclic adenosine monophosphate (cAMP) formation in rat retinal pigment epithelial (RPE) cells, suggesting that K ATP -channel might be involved in the effect of H 2 S on the cAMP-related RPE cell proliferation, apoptosis, and phagocytosis ( Njie-Mbye et al, 2012 ). NaHS was found to have a prominent relaxation effect on the retina arteries by acting on the voltage-dependent potassium channel (K v ) and inwardly rectifying potassium channel (K ir ) ( Takır et al, 2015 ), indicating that H 2 S may play an important role in regulating the retina vascular system.…”

Section: Effect Of H 2 S On Retinal Physiologymentioning

confidence: 99%

“…NF-κB, ERK/MAPK, and JNK/MAPK pathways were involved in the anti-apoptotic mechanisms for H 2 S preconditioning ( Biermann et al, 2011 ). Additionally, H 2 S could relax retinal arteries by targeting on the potassium channel ( Takır et al, 2015 ), which might be involved in the protective effect of H 2 S on the retinal vascular diseases.…”

Section: Effect Of H 2 S On Retinal Pathologymentioning

confidence: 99%

Role of Hydrogen Sulfide in Retinal Diseases

Jin

Yang

2017

Front. Pharmacol.

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As the third gasotransmitter, hydrogen sulfide (H2S) plays a crucial role in the physiology and pathophysiology of many systems in the body, such as the nervous, cardiovascular, respiratory, and gastrointestinal systems. The mechanisms for its effects, including inhibiting ischemic injury, reducing oxidative stress damage, regulating apoptosis, and reducing the inflammation reaction in different systems, have not been fully understood. Recently, H2S and its endogenous synthesis pathway were found in the mammalian retina. This review describes the production and the metabolism of H2S and the evidence of a role of H2S in the retina physiology and in the different retinal diseases, including retinal degenerative diseases and vascular diseases. In the retina, H2S is generated in the presence of cystathionine-β-synthase, cystathionine-γ-lyase, and 3-mercaptopyruvate sulfurtransferase from L-cysteine. The role of endogenous H2S and its physiologic effect in the retina are still elusive. However, strong evidence shows that retina-derived H2S might play protective or deleterious role in the pathogenesis of retinal diseases. For example, by regulating Ca2+ influx, H2S can protect retinal neurons against light-induced degeneration. H2S preconditioning can mediate the anti-apoptotic effect of retinal ganglion cells in retinal ischemia/reperfusion injury. Treatment with H2S in rats relieves diabetic retinopathy by suppressing oxidative stress and reducing inflammation. Further studies would greatly improve our understanding of the pathophysiologic mechanisms responsible for retinal diseases and the potential for the H2S-related therapy of the retinal diseases as well.

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NaHS induces relaxation response in prostaglandin F2α precontracted bovine retinal arteries partially via Kv and Kir channels

Cited by 18 publications

References 33 publications

Hydrogen Sulfide Contributes to Retinal Neovascularization in Ischemia-Induced Retinopathy

Hydrogen Sulfide Contributes to Retinal Neovascularization in Ischemia-Induced Retinopathy

The Retinal Relaxing Factor: Update on an Enigmatic Regulator of the Retinal Circulation

Role of Hydrogen Sulfide in Retinal Diseases

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