Alternatively Spliced Tissue Factor promotes plaque progression, inflammation and angiogenesis in experimental atherosclerosis
DC Field | Value | Language |
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dc.contributor.author | Alicea, Daniel | - |
dc.contributor.author | Chudnovskiy, Aleksey | - |
dc.contributor.author | Rodriguez, David T. | - |
dc.contributor.author | Yang, Dong Kwon | - |
dc.contributor.author | Jeong, Dongtak | - |
dc.contributor.author | Kovacic, Jason C. | - |
dc.contributor.author | Badimon, Juan J. | - |
dc.contributor.author | Weber, Thomas | - |
dc.contributor.author | Merad, Miriam | - |
dc.contributor.author | Najjar, Roger J. | - |
dc.contributor.author | Fuster, Valentin | - |
dc.contributor.author | Giannarelli, Chiara | - |
dc.date.accessioned | 2021-06-22T22:04:57Z | - |
dc.date.available | 2021-06-22T22:04:57Z | - |
dc.date.issued | 2014-11 | - |
dc.identifier.issn | 0009-7322 | - |
dc.identifier.issn | 1524-4539 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/erica/handle/2021.sw.erica/21122 | - |
dc.description.abstract | Introduction: Alternatively Spliced Tissue Factor (asTF) is novel isoform of tissue factor with angiogenic activity mediated via HIF-1α signaling (Giannarelli, AHA 13). asTF is highly expressed in human complicated atherosclerotic plaques (Giannarelli, ACC 13); however, it is unknown whether asTF has a functional role in atherogenesis. Hypothesis: asTF promotes atherosclerotic plaque progression, inflammation and angiogenesis. Methods: ApoE-/- mice (8-weeks old; n=15) were fed a Western-type diet from 2 weeks before surgery continuing through the experiment. Immediately after transluminal wire injury of the left common carotid artery (LCCA), LCCA was incubated with lentivirus encoding asTF-GFP (asTF+ group; n=10) or GFP (asTF- control group; n=5). Four weeks after, blood and spleen were collected for flow cytometry analysis of neutrophils and monocytes. LCCA was removed and processed for H&E, Oil-Red O staining and immunostaining for macrophages (MOMA-2 and MAC-3), vascular smooth muscle cells (VSMC, α-actin), endothelial cells (CD31) and HIF-1α. Results: Neointimal thickness and plaque lipid accumulation were significantly greater in asTF+ vs asTF- mice (Fig 1, A-C). An increase in plaque macrophages, neovessels and HIF-1α was observed in asTF+ vs asTF- (Fig 1, D-F). Medial thickness and VSMC density were similar between groups. Increased circulating neutrophils and Ly6Chigh (classical/inflammatory) monocytes were observed in asTF+ vs asTF- mice (Fig 1, G,H). In contrast, circulating Ly6Clow (patrolling) monocytes were significantly reduced (Fig 1, I). Similar findings were observed in the spleen (Fig 1, J-L). Conclusions: Our results demonstrate that asTF expressed within atherosclerotic lesions promotes plaque progression towards a more advanced phenotype and is associated with systemic proinflammatory status. These data makes asTF an attractive marker of plaque vulnerability and a potential therapeutic target for plaque stabilization. | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | Lippincott Williams & Wilkins Ltd. | - |
dc.title | Alternatively Spliced Tissue Factor promotes plaque progression, inflammation and angiogenesis in experimental atherosclerosis | - |
dc.type | Article | - |
dc.publisher.location | 미국 | - |
dc.identifier.doi | 10.1161/circ.130.suppl_2.16942 | - |
dc.identifier.wosid | 000209800306004 | - |
dc.identifier.bibliographicCitation | Circulation, v.130 | - |
dc.citation.title | Circulation | - |
dc.citation.volume | 130 | - |
dc.type.docType | Meeting Abstract | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | sci | - |
dc.description.journalRegisteredClass | scie | - |
dc.relation.journalResearchArea | Cardiovascular System & Cardiology | - |
dc.relation.journalWebOfScienceCategory | Cardiac & Cardiovascular Systems | - |
dc.relation.journalWebOfScienceCategory | Peripheral Vascular Disease | - |
dc.subject.keywordAuthor | Tissue factor | - |
dc.subject.keywordAuthor | Inflammation | - |
dc.subject.keywordAuthor | Atherosclerosis | - |
dc.subject.keywordAuthor | Vulnerable plaque | - |
dc.subject.keywordAuthor | Gene transfer | - |
dc.identifier.url | https://www.ahajournals.org/doi/10.1161/circ.130.suppl_2.16942 | - |
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