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Conference Paper: Telomere-independent Rap1, modulates NF-kB-dependent inflammation in macrophages
Title | Telomere-independent Rap1, modulates NF-kB-dependent inflammation in macrophages |
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Authors | |
Keywords | Rap1 NF-κB Macrophage Inflammation Atherosclerosis |
Issue Date | 2013 |
Publisher | Nature 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? |
Abstract | AIM: 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. |
Description | This 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 Identifier | http://hdl.handle.net/10722/191707 |
ISSN | 2023 Impact Factor: 6.9 2023 SCImago Journal Rankings: 1.882 |
DC Field | Value | Language |
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dc.contributor.author | Cai, Y | en_US |
dc.contributor.author | Vanhoutte, PM | en_US |
dc.contributor.author | Tang, EHC | en_US |
dc.date.accessioned | 2013-10-15T07:20:21Z | - |
dc.date.available | 2013-10-15T07:20:21Z | - |
dc.date.issued | 2013 | en_US |
dc.identifier.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 | en_US |
dc.identifier.issn | 1671-4083 | - |
dc.identifier.uri | http://hdl.handle.net/10722/191707 | - |
dc.description | This 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.description | Open Access Journal | - |
dc.description | Section 11: CPS-HKPS Young Investigators Awards for PhD Students: abstract S11.3 | - |
dc.description.abstract | AIM: 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.language | eng | en_US |
dc.publisher | Nature Publishing Group. The Journal's web site is located at http://www.nature.com/aps/index.html | - |
dc.relation.ispartof | Acta Pharmacologica Sinica | en_US |
dc.subject | Rap1 | - |
dc.subject | NF-κB | - |
dc.subject | Macrophage | - |
dc.subject | Inflammation | - |
dc.subject | Atherosclerosis | - |
dc.title | Telomere-independent Rap1, modulates NF-kB-dependent inflammation in macrophages | en_US |
dc.type | Conference_Paper | en_US |
dc.identifier.email | Vanhoutte, PM: vanhoutt@hku.hk | en_US |
dc.identifier.email | Tang, EHC: evatang1@hku.hk | en_US |
dc.identifier.authority | Vanhoutte, PM=rp00238 | en_US |
dc.identifier.authority | Tang, EHC=rp01382 | en_US |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.hkuros | 225362 | en_US |
dc.identifier.volume | 34 | - |
dc.identifier.issue | suppl. | - |
dc.publisher.place | United States | - |
dc.customcontrol.immutable | sml 131111 | - |
dc.identifier.issnl | 1671-4083 | - |