Please use this identifier to cite or link to this item: https://doi.org/10.1177/1759091415578711
Title: Cystathionine ?-synthase inhibition is a potential therapeutic approach to treatment of ischemic injury
Authors: Chan, S.J 
Chai, C 
Lim, T.W
Yamamoto, M 
Lo, E.H
Lai, M.K.P 
Wong, P.T.H 
Keywords: cystathionine beta synthase
cysteine
homocysteine
hydrogen sulfide
neuron specific nuclear protein
aminooxyacetic acid
cystathionine beta synthase
enzyme inhibitor
glucose
animal cell
animal experiment
animal model
animal tissue
Article
astrocyte
cell death
cell viability
controlled study
human
human cell
hypoxic ischemic encephalopathy
immunofluorescence test
male
MTT assay
nonhuman
protein expression
protein localization
rat
upregulation
Western blotting
animal
antagonists and inhibitors
brain
brain ischemia
cell culture
cell hypoxia
cell survival
cerebral artery disease
deficiency
disease model
drug effects
genetics
metabolism
pathology
PC12 cell line
physiology
Sprague Dawley rat
tumor cell line
Aminooxyacetic Acid
Animals
Astrocytes
Brain
Brain Ischemia
Cell Hypoxia
Cell Line, Tumor
Cell Survival
Cells, Cultured
Cystathionine beta-Synthase
Disease Models, Animal
Enzyme Inhibitors
Glucose
Humans
Hydrogen Sulfide
Infarction, Middle Cerebral Artery
PC12 Cells
Rats
Rats, Sprague-Dawley
Issue Date: 2015
Citation: Chan, S.J, Chai, C, Lim, T.W, Yamamoto, M, Lo, E.H, Lai, M.K.P, Wong, P.T.H (2015). Cystathionine ?-synthase inhibition is a potential therapeutic approach to treatment of ischemic injury. ASN Neuro 7 (2). ScholarBank@NUS Repository. https://doi.org/10.1177/1759091415578711
Abstract: Hydrogen sulfide (H2S) has been reported to exacerbate stroke outcome in experimental models. Cystathionine ?-synthase (CBS) has been implicated as the predominant H2S-producing enzyme in central nervous system. When SH-SY5Y cells were transfected to overexpress CBS, these cells were able to synthesize H2S when exposed to high levels of enzyme substrates but not substrate concentrations that may reflect normal physiological conditions. At the same time, these cells demon-strated exacerbated cell death when subjected to oxygen and glucose deprivation (OGD) together with high substrate concentrations, indicating that H2S production has a detrimental effect on cell survival. This effect could be abolished by CBS inhibition. The same effect was observed with primary astrocytes exposed to OGD and high substrates or sodium hydro-sulfide. In addition, CBS was upregulated and activated by truncation in primary astrocytes subjected to OGD. When rats were subjected to permanent middle cerebral artery occlusion, CBS activation was also observed. These results imply that in acute ischemic conditions, CBS is upregulated and activated by truncation causing an increased production of H2S, which exacerbate the ischemic injuries. Therefore, CBS inhibition may be a viable approach to stroke treatment. © The Author(s) 2015 Reprints and permissions.
Source Title: ASN Neuro
URI: https://scholarbank.nus.edu.sg/handle/10635/174141
ISSN: 17590914
DOI: 10.1177/1759091415578711
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