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Conference Paper: Telomere-independent Rap1, modulates NF-kB-dependent inflammation in macrophages

TitleTelomere-independent Rap1, modulates NF-kB-dependent inflammation in macrophages
Authors
KeywordsRap1
NF-κB
Macrophage
Inflammation
Atherosclerosis
Issue Date2013
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/aps/index.html
Citation
The 12th Meeting of the Asia Pacific Federation of Pharmacologists (APFPM) & Joint Meeting of Pharmacology of Chinese Pharmacological Society and Hong Kong Pharmacology Society, Shanghai, July 9-13, 2013. In Acta Pharmacologica Sinica, 2013, v. 34 suppl., abstract S11.3 How to Cite?
AbstractAIM: The activity of nuclear factor (NF-κB) is modulated by cytoplasmic repressor activator protein 1 (Rap1) in cancel cells. Experiments were designed to test whether or not Rap1 is present in atheromatous lesions and affects NF-κB dependent inflammation in macrophages, the predominant cell type involved in the progression of atherosclerotic lesions. METHODS: The expression of Rap1 and macrophages in human atheromatous lesions was detected by immunohistochemistry. The expression of lipopolysaccharide- (LPS, 50 ng/mL, 4 h) and tumor necrosis factor alpha (TNF-α, 100 ng/mL, 4 h) induced NF-κB dependent genes and proteins in wild type and Rap1 knockdown THP-1 cells were measured using real-time PCR and enzyme-linked immune sorbent assays. Western blotting was applied to determine the expression of p65 and its phosphorylation in wild type and Rap1 knockdown THP-1 cells. RESULTS: Rap1 co-localized with macrophages and its staining positively correlated with graded human atherosclerosis. In THP-1 cells, Rap1 knockdown suppressed the phosphorylation of p65 and reduced the expression of LPS- or TNFα-induced NF-κB dependent pro-inflammatory cytokines at mRNA and protein levels. CONCLUSION: Telomere-independent Rap1 is present in human athermanous lesions. Cytoplasmic Rap1 within macrophages may impact on inflammation during atherosclerosis.
DescriptionThis journal suppl. contain abstracts of: The 12th APFPM Meeting ; The 2nd Joint Symposium on Pharmacology of Chinese Pharmacological Society and British Pharmacological Society ; The 2013 Joint Meeting of Pharmacology of Chinese Pharmacological Society and Hong Kong Pharmacology Society and The 12th Conference of Chinese Pharmacological Society
Open Access Journal
Section 11: CPS-HKPS Young Investigators Awards for PhD Students: abstract S11.3
Persistent Identifierhttp://hdl.handle.net/10722/191707
ISSN
2015 Impact Factor: 3.166
2015 SCImago Journal Rankings: 1.161

 

DC FieldValueLanguage
dc.contributor.authorCai, Yen_US
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorTang, EHCen_US
dc.date.accessioned2013-10-15T07:20:21Z-
dc.date.available2013-10-15T07:20:21Z-
dc.date.issued2013en_US
dc.identifier.citationThe 12th Meeting of the Asia Pacific Federation of Pharmacologists (APFPM) & Joint Meeting of Pharmacology of Chinese Pharmacological Society and Hong Kong Pharmacology Society, Shanghai, July 9-13, 2013. In Acta Pharmacologica Sinica, 2013, v. 34 suppl., abstract S11.3en_US
dc.identifier.issn1671-4083-
dc.identifier.urihttp://hdl.handle.net/10722/191707-
dc.descriptionThis journal suppl. contain abstracts of: The 12th APFPM Meeting ; The 2nd Joint Symposium on Pharmacology of Chinese Pharmacological Society and British Pharmacological Society ; The 2013 Joint Meeting of Pharmacology of Chinese Pharmacological Society and Hong Kong Pharmacology Society and The 12th Conference of Chinese Pharmacological Society-
dc.descriptionOpen Access Journal-
dc.descriptionSection 11: CPS-HKPS Young Investigators Awards for PhD Students: abstract S11.3-
dc.description.abstractAIM: The activity of nuclear factor (NF-κB) is modulated by cytoplasmic repressor activator protein 1 (Rap1) in cancel cells. Experiments were designed to test whether or not Rap1 is present in atheromatous lesions and affects NF-κB dependent inflammation in macrophages, the predominant cell type involved in the progression of atherosclerotic lesions. METHODS: The expression of Rap1 and macrophages in human atheromatous lesions was detected by immunohistochemistry. The expression of lipopolysaccharide- (LPS, 50 ng/mL, 4 h) and tumor necrosis factor alpha (TNF-α, 100 ng/mL, 4 h) induced NF-κB dependent genes and proteins in wild type and Rap1 knockdown THP-1 cells were measured using real-time PCR and enzyme-linked immune sorbent assays. Western blotting was applied to determine the expression of p65 and its phosphorylation in wild type and Rap1 knockdown THP-1 cells. RESULTS: Rap1 co-localized with macrophages and its staining positively correlated with graded human atherosclerosis. In THP-1 cells, Rap1 knockdown suppressed the phosphorylation of p65 and reduced the expression of LPS- or TNFα-induced NF-κB dependent pro-inflammatory cytokines at mRNA and protein levels. CONCLUSION: Telomere-independent Rap1 is present in human athermanous lesions. Cytoplasmic Rap1 within macrophages may impact on inflammation during atherosclerosis.-
dc.languageengen_US
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/aps/index.html-
dc.relation.ispartofActa Pharmacologica Sinicaen_US
dc.subjectRap1-
dc.subjectNF-κB-
dc.subjectMacrophage-
dc.subjectInflammation-
dc.subjectAtherosclerosis-
dc.titleTelomere-independent Rap1, modulates NF-kB-dependent inflammation in macrophagesen_US
dc.typeConference_Paperen_US
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_US
dc.identifier.emailTang, EHC: evatang1@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.identifier.authorityTang, EHC=rp01382en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros225362en_US
dc.identifier.volume34-
dc.identifier.issuesuppl.-
dc.publisher.placeUnited States-
dc.customcontrol.immutablesml 131111-

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