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Conference Paper: Stimulation of endothelial ecto 5′-nucleotidase by lipopolysaccharides via phosphatidylinositol-3 pathway

TitleStimulation of endothelial ecto 5′-nucleotidase by lipopolysaccharides via phosphatidylinositol-3 pathway
Authors
Issue Date2008
PublisherFederation of American Societies for Experimental Biology. Meeting abstracts can be accessed via http://www.fasebj.org/search.dtl
Citation
Experimental Biology 2008 - ASPET's Centennial Meeting, San Diego, CA, 5-9 April 2008. In The FASEB Journal, 2008, v. 22 n. 1S, p. 1128.14 How to Cite?
AbstractInflammation of endothelium is associated with atherosclerosis. It is known that adenosine possesses anti-inflammatory function and its level is increased at the sites of inflammation. The mechanism underlying the increased adenosine level is not fully understood. Therefore, we studied the effect of inflammation on endothelial ecto-5’nucleotidase (ecto-5’Nu), an enzyme which metabolizes extracellular adenosine monophosphate into adenosine. Lipopolysaccharide (LPS) was used to induce inflammation of human umbilical vein endothelial cells (HUVEC). Biochemical assay revealed that the ecto-5’Nu activity in HUVEC was stimulated by LPS after 24 hr treatment. RT-PCR showed that mRNA expression of ecto-5’Nu was not changed but western blot showed that its protein expression was increased by LPS. In addition, LY294-002, a phosphatidylinositol 3-kinase (PI3K) inhibitor, reduced the LPS-stimulated ecto-5’Nu activity but ammonium pyrrolidine dithiocarbamate (APDC), a NF-êB inhibitor, had no effect. The stimulation of ecto-5’Nu by LPS was unaltered when HUVEC was incubated in 25 mM glucose, a condition which mimics the hyperglycemia of diabetes. In conclusion, it is suggested that the increased extracellular adenosine level during inflammation may be related to increased translational regulation of ecto-5’Nu through a PI3K signaling pathway and this mechanism may not be affected in diabetes.
Persistent Identifierhttp://hdl.handle.net/10722/106833
ISSN
2015 Impact Factor: 5.299
2015 SCImago Journal Rankings: 2.775

 

DC FieldValueLanguage
dc.contributor.authorLeung, GPHen_HK
dc.contributor.authorMan, RYKen_HK
dc.contributor.authorVanhoutte, PMGRen_HK
dc.contributor.authorLi, RWSen_HK
dc.date.accessioned2010-09-25T23:32:19Z-
dc.date.available2010-09-25T23:32:19Z-
dc.date.issued2008en_HK
dc.identifier.citationExperimental Biology 2008 - ASPET's Centennial Meeting, San Diego, CA, 5-9 April 2008. In The FASEB Journal, 2008, v. 22 n. 1S, p. 1128.14-
dc.identifier.issn0892-6638en_HK
dc.identifier.urihttp://hdl.handle.net/10722/106833-
dc.description.abstractInflammation of endothelium is associated with atherosclerosis. It is known that adenosine possesses anti-inflammatory function and its level is increased at the sites of inflammation. The mechanism underlying the increased adenosine level is not fully understood. Therefore, we studied the effect of inflammation on endothelial ecto-5’nucleotidase (ecto-5’Nu), an enzyme which metabolizes extracellular adenosine monophosphate into adenosine. Lipopolysaccharide (LPS) was used to induce inflammation of human umbilical vein endothelial cells (HUVEC). Biochemical assay revealed that the ecto-5’Nu activity in HUVEC was stimulated by LPS after 24 hr treatment. RT-PCR showed that mRNA expression of ecto-5’Nu was not changed but western blot showed that its protein expression was increased by LPS. In addition, LY294-002, a phosphatidylinositol 3-kinase (PI3K) inhibitor, reduced the LPS-stimulated ecto-5’Nu activity but ammonium pyrrolidine dithiocarbamate (APDC), a NF-êB inhibitor, had no effect. The stimulation of ecto-5’Nu by LPS was unaltered when HUVEC was incubated in 25 mM glucose, a condition which mimics the hyperglycemia of diabetes. In conclusion, it is suggested that the increased extracellular adenosine level during inflammation may be related to increased translational regulation of ecto-5’Nu through a PI3K signaling pathway and this mechanism may not be affected in diabetes.-
dc.languageengen_HK
dc.publisherFederation of American Societies for Experimental Biology. Meeting abstracts can be accessed via http://www.fasebj.org/search.dtlen_HK
dc.relation.ispartofThe FASEB Journalen_HK
dc.titleStimulation of endothelial ecto 5′-nucleotidase by lipopolysaccharides via phosphatidylinositol-3 pathwayen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0176-8638&volume=&spage=&epage=&date=2008&atitle=Stimulation+of+endothelial+ecto+5’-nucleotidase+by+lipopolysaccharides+via+phosphatidylinositol-3+pathwayen_HK
dc.identifier.emailLeung, GPH: leung_pak_heng@hotmail.comen_HK
dc.identifier.emailMan, RYK: rykman@hkucc.hku.hken_HK
dc.identifier.emailVanhoutte, PMGR: vanhoutt@hku.hken_HK
dc.identifier.emailLi, RWS: h0594069@hkusua.hku.hken_HK
dc.identifier.authorityLeung, GPH=rp00234en_HK
dc.identifier.authorityMan, RYK=rp00236en_HK
dc.identifier.hkuros143138en_HK

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