Fibroblast activation protein is induced by inflammation and degrades type I collagen in thin-cap fibroatheromata
Collagen degradation in atherosclerotic plaques with thin fibrous caps renders them more prone to rupture. Fibroblast activation protein (FAP) plays a role in arthritis and tumour formation through its collagenase activity. However, the significance of FAP in thin-cap human fibroatheromata remains u...
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| Hauptverfasser: | , , , , , , , , , , , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
02 February 2011
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| In: |
European heart journal
Year: 2011, Jahrgang: 32, Heft: 21, Pages: 2713-2722 |
| ISSN: | 1522-9645 |
| DOI: | 10.1093/eurheartj/ehq519 |
| Online-Zugang: | Resolving-System, kostenfrei, Volltext: https://doi.org/10.1093/eurheartj/ehq519
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| Verfasserangaben: | Chad E. Brokopp, Roman Schoenauer, Peter Richards, Stefan Bauer, Christine Lohmann, Maximilian Y. Emmert, Benedikt Weber, Stephan Winnik, Elena Aikawa, Kirk Graves, Michele Genoni, Peter Vogt, Thomas F. Lüscher, Christoph Renner, Simon P. Hoerstrup, and Christian M. Matter |
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| 245 | 1 | 0 | |a Fibroblast activation protein is induced by inflammation and degrades type I collagen in thin-cap fibroatheromata |c Chad E. Brokopp, Roman Schoenauer, Peter Richards, Stefan Bauer, Christine Lohmann, Maximilian Y. Emmert, Benedikt Weber, Stephan Winnik, Elena Aikawa, Kirk Graves, Michele Genoni, Peter Vogt, Thomas F. Lüscher, Christoph Renner, Simon P. Hoerstrup, and Christian M. Matter |
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| 520 | |a Collagen degradation in atherosclerotic plaques with thin fibrous caps renders them more prone to rupture. Fibroblast activation protein (FAP) plays a role in arthritis and tumour formation through its collagenase activity. However, the significance of FAP in thin-cap human fibroatheromata remains unknown.We detected enhanced FAP expression in type IV-V human aortic atheromata (n = 12), compared with type II-III lesions (n = 9; P < 0.01) and healthy aortae (n = 8; P < 0.01) by immunostaining and western blot analyses. Fibroblast activation protein was also increased in thin-cap (<65 µm) vs. thick-cap (≥65 µm) human coronary fibroatheromata (n = 12; P < 0.01). Fibroblast activation protein was expressed by human aortic smooth muscle cells (HASMC) as shown by colocalization on immunofluorescent aortic plaque stainings (n = 10; P < 0.01) and by flow cytometry in cell culture. Although macrophages did not express FAP, macrophage burden in human aortic plaques correlated with FAP expression (n = 12; R2= 0.763; P < 0.05). Enzyme-linked immunosorbent assays showed a time- and dose-dependent up-regulation of FAP in response to human tumour necrosis factor α (TNFα) in HASMC (n = 6; P < 0.01). Moreover, supernatants from peripheral blood-derived macrophages induced FAP expression in cultured HASMC (n = 6; P < 0.01), an effect abolished by blocking TNFα (n = 6; P < 0.01). Fibroblast activation protein associated with collagen-poor regions in human coronary fibrous caps and digested type I collagen and gelatin in vitro (n = 6; P < 0.01). Zymography revealed that FAP-mediated collagenase activity was neutralized by an antibody directed against the FAP catalytic domain both in HASMC (n = 6; P < 0.01) and in fibrous caps of atherosclerotic plaques (n = 10; P < 0.01).Fibroblast activation protein expression in HASMC is induced by macrophage-derived TNFα. Fibroblast activation protein associates with thin-cap human coronary fibroatheromata and contributes to type I collagen breakdown in fibrous caps. | ||
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