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Hydrogen Sulfide Contributes to Retinal Neovascularization in Ischemia-Induced Retinopathy.
Invest Ophthalmol Vis Sci. 2016 06 01; 57(7):3002-9.IO

Abstract

PURPOSE

Hydrogen 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.

METHODS

Studies 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.

RESULTS

Hydrogen 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.

CONCLUSIONS

Our 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.

Authors+Show Affiliations

Center for Biomedical Engineering, The University of Texas Medical Branch, Galveston, Texas, United States 2Department of Ophthalmology and Visual Sciences, The University of Texas Medical Branch, Galveston, Texas, United States 3Neuroscience & Cell Biolo.Anesthesiology, The University of Texas Medical Branch, Galveston, Texas, United States.Department of Ophthalmology and Visual Sciences, The University of Texas Medical Branch, Galveston, Texas, United States.Department of Ophthalmology and Visual Sciences, The University of Texas Medical Branch, Galveston, Texas, United States.Center for Biomedical Engineering, The University of Texas Medical Branch, Galveston, Texas, United States.Department of Ophthalmology and Visual Sciences, The University of Texas Medical Branch, Galveston, Texas, United States.Pharmacology and Toxicology, The University of Texas Medical Branch, Galveston, Texas, United States.Anesthesiology, The University of Texas Medical Branch, Galveston, Texas, United States.Department of Ophthalmology and Visual Sciences, The University of Texas Medical Branch, Galveston, Texas, United States 3Neuroscience & Cell Biology, The University of Texas Medical Branch, Galveston, Texas, United States.Center for Biomedical Engineering, The University of Texas Medical Branch, Galveston, Texas, United States 2Department of Ophthalmology and Visual Sciences, The University of Texas Medical Branch, Galveston, Texas, United States.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

27273718

Citation

Gersztenkorn, David, et al. "Hydrogen Sulfide Contributes to Retinal Neovascularization in Ischemia-Induced Retinopathy." Investigative Ophthalmology & Visual Science, vol. 57, no. 7, 2016, pp. 3002-9.
Gersztenkorn D, Coletta C, Zhu S, et al. Hydrogen Sulfide Contributes to Retinal Neovascularization in Ischemia-Induced Retinopathy. Invest Ophthalmol Vis Sci. 2016;57(7):3002-9.
Gersztenkorn, D., Coletta, C., Zhu, S., Ha, Y., Liu, H., Tie, H., Zhou, J., Szabo, C., Zhang, W., & Motamedi, M. (2016). Hydrogen Sulfide Contributes to Retinal Neovascularization in Ischemia-Induced Retinopathy. Investigative Ophthalmology & Visual Science, 57(7), 3002-9. https://doi.org/10.1167/iovs.15-18555
Gersztenkorn D, et al. Hydrogen Sulfide Contributes to Retinal Neovascularization in Ischemia-Induced Retinopathy. Invest Ophthalmol Vis Sci. 2016 06 1;57(7):3002-9. PubMed PMID: 27273718.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Hydrogen Sulfide Contributes to Retinal Neovascularization in Ischemia-Induced Retinopathy. AU - Gersztenkorn,David, AU - Coletta,Ciro, AU - Zhu,Shuang, AU - Ha,Yonju, AU - Liu,Hua, AU - Tie,Hongyan, AU - Zhou,Jia, AU - Szabo,Csaba, AU - Zhang,Wenbo, AU - Motamedi,Massoud, PY - 2016/6/9/entrez PY - 2016/6/9/pubmed PY - 2017/6/20/medline SP - 3002 EP - 9 JF - Investigative ophthalmology & visual science JO - Invest Ophthalmol Vis Sci VL - 57 IS - 7 N2 - PURPOSE: Hydrogen 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. METHODS: Studies 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. RESULTS: Hydrogen 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. CONCLUSIONS: Our 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. SN - 1552-5783 UR - https://www.unboundmedicine.com/medline/citation/27273718/Hydrogen_Sulfide_Contributes_to_Retinal_Neovascularization_in_Ischemia_Induced_Retinopathy_ DB - PRIME DP - Unbound Medicine ER -