Astrocytes produce the antiinflammatory and neuroprotective agent hydrogen sulfide.
Identifieur interne : 002031 ( Main/Merge ); précédent : 002030; suivant : 002032Astrocytes produce the antiinflammatory and neuroprotective agent hydrogen sulfide.
Auteurs : Moonhee Lee [Canada] ; Claudia Schwab ; Sheng Yu ; Edith Mcgeer ; Patrick L. McgeerSource :
- Neurobiology of aging [ 1558-1497 ] ; 2009.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Alkynes (pharmacology), Astrocytes (enzymology), Astrocytes (immunology), Astrocytes (metabolism), Brain (enzymology), Brain (immunology), Brain (metabolism), Cell Line, Tumor, Cells, Cultured, Cystathionine beta-Synthase (antagonists & inhibitors), Cystathionine beta-Synthase (metabolism), Cystathionine gamma-Lyase (antagonists & inhibitors), Cystathionine gamma-Lyase (metabolism), Enzyme Inhibitors (pharmacology), Female, Glycine (analogs & derivatives), Glycine (pharmacology), Humans, Hydrogen Sulfide (metabolism), Hydroxylamine (pharmacology), Interleukin-6 (metabolism), Male, Microglia (enzymology), Microglia (immunology), Microglia (metabolism), NF-kappa B (metabolism), Neuroprotective Agents (metabolism), Nitrites (metabolism), Tumor Necrosis Factor-alpha (metabolism).
- MESH :
- chemical , analogs & derivatives : Glycine.
- chemical , antagonists & inhibitors : Cystathionine beta-Synthase, Cystathionine gamma-Lyase.
- chemical , metabolism : Cystathionine beta-Synthase, Cystathionine gamma-Lyase, Hydrogen Sulfide, Interleukin-6, NF-kappa B, Neuroprotective Agents, Nitrites, Tumor Necrosis Factor-alpha.
- chemical , pharmacology : Alkynes, Enzyme Inhibitors, Glycine, Hydroxylamine.
- enzymology : Astrocytes, Brain, Microglia.
- immunology : Astrocytes, Brain, Microglia.
- metabolism : Astrocytes, Brain, Microglia.
- Aged, Aged, 80 and over, Cell Line, Tumor, Cells, Cultured, Female, Humans, Male.
Abstract
Hydrogen sulfide (H(2)S) is an essential physiological product in brain. We investigated the expression of cystathionine-beta-synthase (CBS) and cystathionine-gamma-lyase (CGL), the two H(2)S synthesizing enzymes, in human cell lines and in human brain. Only astrocytes were strongly immunostained for CBS. Cultured astrocytes synthesized H(2)S at the rate of 15.06 micromol/g protein/h, which was 7.57 fold higher than microglial cells, 10.27 fold higher than SH-SY5Y cells and 11.32 fold higher than NT-2 cells. The H(2)S synthesis in all these cell types was inhibited by the CBS inhibitor hydroxylamine, but not by the CGL inhibitor propargylglycine (PAG). Synthesis of H(2)S by HUVEC cells was inhibited by PAG but not by hydroxylamine indicating that these vascular cells utilize CGL but not CBS. Inflammatory activation of microglia and astrocytes caused induction of NFkappaB, release of the inflammatory mediators TNFalpha, IL-6 and nitrite ions, down-regulation of CBS, and down-regulation of H(2)S synthesis. There was no effect of such treatment on HUVEC cells. The effects were partially reversed by pretreatment of cells with the H(2)S releasing agent NaSH. These data indicate that H(2)S is an endogenous antiinflammatory and neuroprotective agent under the synthetic control of CBS. H(2)S releasing drugs may have therapeutic potential in neurodegenerative disorders of aging such as Alzheimer disease and Parkinson disease.
DOI: 10.1016/j.neurobiolaging.2009.06.001
PubMed: 19631409
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pubmed:19631409Le document en format XML
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Mcgeer</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2009">2009</date><idno type="RBID">pubmed:19631409</idno><idno type="pmid">19631409</idno><idno type="doi">10.1016/j.neurobiolaging.2009.06.001</idno><idno type="wicri:Area/PubMed/Corpus">000E36</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000E36</idno><idno type="wicri:Area/PubMed/Curation">000E36</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000E36</idno><idno type="wicri:Area/PubMed/Checkpoint">000E36</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000E36</idno><idno type="wicri:Area/Ncbi/Merge">000B20</idno><idno type="wicri:Area/Ncbi/Curation">000B20</idno><idno type="wicri:Area/Ncbi/Checkpoint">000B20</idno><idno type="wicri:Area/Main/Merge">002031</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Astrocytes produce the antiinflammatory and neuroprotective agent hydrogen sulfide.</title><author><name sortKey="Lee, Moonhee" sort="Lee, Moonhee" uniqKey="Lee M" first="Moonhee" last="Lee">Moonhee Lee</name><affiliation wicri:level="1"><nlm:affiliation>Kinsmen Laboratory of Neurological Research, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Kinsmen Laboratory of Neurological Research, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC</wicri:regionArea><wicri:noRegion>BC</wicri:noRegion></affiliation></author><author><name sortKey="Schwab, Claudia" sort="Schwab, Claudia" uniqKey="Schwab C" first="Claudia" last="Schwab">Claudia Schwab</name></author><author><name sortKey="Yu, Sheng" sort="Yu, Sheng" uniqKey="Yu S" first="Sheng" last="Yu">Sheng Yu</name></author><author><name sortKey="Mcgeer, Edith" sort="Mcgeer, Edith" uniqKey="Mcgeer E" first="Edith" last="Mcgeer">Edith Mcgeer</name></author><author><name sortKey="Mcgeer, Patrick L" sort="Mcgeer, Patrick L" uniqKey="Mcgeer P" first="Patrick L" last="Mcgeer">Patrick L. Mcgeer</name></author></analytic><series><title level="j">Neurobiology of aging</title><idno type="eISSN">1558-1497</idno><imprint><date when="2009" type="published">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Alkynes (pharmacology)</term><term>Astrocytes (enzymology)</term><term>Astrocytes (immunology)</term><term>Astrocytes (metabolism)</term><term>Brain (enzymology)</term><term>Brain (immunology)</term><term>Brain (metabolism)</term><term>Cell Line, Tumor</term><term>Cells, Cultured</term><term>Cystathionine beta-Synthase (antagonists & inhibitors)</term><term>Cystathionine beta-Synthase (metabolism)</term><term>Cystathionine gamma-Lyase (antagonists & inhibitors)</term><term>Cystathionine gamma-Lyase (metabolism)</term><term>Enzyme Inhibitors (pharmacology)</term><term>Female</term><term>Glycine (analogs & derivatives)</term><term>Glycine (pharmacology)</term><term>Humans</term><term>Hydrogen Sulfide (metabolism)</term><term>Hydroxylamine (pharmacology)</term><term>Interleukin-6 (metabolism)</term><term>Male</term><term>Microglia (enzymology)</term><term>Microglia (immunology)</term><term>Microglia (metabolism)</term><term>NF-kappa B (metabolism)</term><term>Neuroprotective Agents (metabolism)</term><term>Nitrites (metabolism)</term><term>Tumor Necrosis Factor-alpha (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Glycine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Cystathionine beta-Synthase</term><term>Cystathionine gamma-Lyase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cystathionine beta-Synthase</term><term>Cystathionine gamma-Lyase</term><term>Hydrogen Sulfide</term><term>Interleukin-6</term><term>NF-kappa B</term><term>Neuroprotective Agents</term><term>Nitrites</term><term>Tumor Necrosis Factor-alpha</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Alkynes</term><term>Enzyme Inhibitors</term><term>Glycine</term><term>Hydroxylamine</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Astrocytes</term><term>Brain</term><term>Microglia</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Astrocytes</term><term>Brain</term><term>Microglia</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Astrocytes</term><term>Brain</term><term>Microglia</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Cell Line, Tumor</term><term>Cells, Cultured</term><term>Female</term><term>Humans</term><term>Male</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Hydrogen sulfide (H(2)S) is an essential physiological product in brain. We investigated the expression of cystathionine-beta-synthase (CBS) and cystathionine-gamma-lyase (CGL), the two H(2)S synthesizing enzymes, in human cell lines and in human brain. Only astrocytes were strongly immunostained for CBS. Cultured astrocytes synthesized H(2)S at the rate of 15.06 micromol/g protein/h, which was 7.57 fold higher than microglial cells, 10.27 fold higher than SH-SY5Y cells and 11.32 fold higher than NT-2 cells. The H(2)S synthesis in all these cell types was inhibited by the CBS inhibitor hydroxylamine, but not by the CGL inhibitor propargylglycine (PAG). Synthesis of H(2)S by HUVEC cells was inhibited by PAG but not by hydroxylamine indicating that these vascular cells utilize CGL but not CBS. Inflammatory activation of microglia and astrocytes caused induction of NFkappaB, release of the inflammatory mediators TNFalpha, IL-6 and nitrite ions, down-regulation of CBS, and down-regulation of H(2)S synthesis. There was no effect of such treatment on HUVEC cells. The effects were partially reversed by pretreatment of cells with the H(2)S releasing agent NaSH. These data indicate that H(2)S is an endogenous antiinflammatory and neuroprotective agent under the synthetic control of CBS. H(2)S releasing drugs may have therapeutic potential in neurodegenerative disorders of aging such as Alzheimer disease and Parkinson disease.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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