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dc.contributor.author
Willecke, Florian
dc.contributor.author
Tiwari, Shilpa
dc.contributor.author
Rupprecht, Benjamin
dc.contributor.author
Wolf, Dennis
dc.contributor.author
Hergeth, Sonja
dc.contributor.author
Hoppe, Natalie
dc.contributor.author
Dufner, Bianca
dc.contributor.author
Schulte, Lisa
dc.contributor.author
Anto Michel, Nathaly
dc.contributor.author
Bukosza, Nora
dc.contributor.author
Marchini, Timoteo Oscar
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dc.contributor.author
Jäekel, Markus
dc.contributor.author
Stachon, Peter
dc.contributor.author
Hilgendorf, Ingo
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Zeschky, Katharina
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Schleicher, Rebecca
dc.contributor.author
Langer, Harald
dc.contributor.author
von zur Muhlen, Constantin
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Bode, Christoph
dc.contributor.author
Karlheinz, Peter
dc.contributor.author
Zirlik, Andreas
dc.date.available
2018-12-27T18:33:12Z
dc.date.issued
2014-08
dc.identifier.citation
Willecke, Florian; Tiwari, Shilpa; Rupprecht, Benjamin ; Wolf, Dennis; Hergeth, Sonja; et al.; Interruption of classic CD40L-CD40 signalling but not of the novel CD40L-Mac-1 interaction limits arterial neointima formation in mice; Schattauer Gmbh-Verlag Medizin Naturwissenschaften; Thrombosis and Haemostasis; 112; 2; 8-2014; 379-389
dc.identifier.issn
0340-6245
dc.identifier.uri
http://hdl.handle.net/11336/67090
dc.description.abstract
The co-stimulatory immune molecule CD40L figures prominently in a variety of inflammatory conditions including arterial disease. Recently, we made the surprising finding that CD40L mediates atherogenesis independently of its classic receptor CD40 via a novel interaction with the leukocyte integrin Mac-1. Here, we hypothesised that selective blockade of the CD40L-Mac-1 interaction may also retard restenosis. We induced neointima formation in C57/BL6 mice by ligation of the left carotid artery. Mice were randomised to daily intraperitoneal injections of either cM7, a small peptide selectively inhibiting the CD40L-Mac-1 interaction, scM7, a scrambled control peptide, or saline for 28 days. Interestingly, cM7-treated mice developed neointima of similar size compared with mice receiving the control peptide or saline as assessed by computer-assisted analysis of histological cross sections. These data demonstrate that the CD40L-Mac-1 interaction is not required for the development of restenosis. In contrast, CD40-deficient mice subjected to carotid ligation in parallel, developed significantly reduced neointimal lesions compared with respective wild-type controls (2872 ± 843 μm2 vs 35469 ± 11870 μm2). Flow cytometry in CD40-deficient mice revealed reduced formation of platelet-granulocyte and platelet-inflammatory monocyte- aggregates. In vitro, supernatants of CD40-deficient platelet-leukocyte aggregates attenuated proliferation and increased apoptosis of smooth muscle cells. Unlike in the setting of atherosclerosis, CD40L mediates neointima formation via its classic receptor CD40 rather than via its recently described novel interaction with Mac-1. Therefore, selective targeting of CD40L-Mac-1 binding does not appear to be a favorable strategy to fight restenosis. © Schattauer 2014.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Schattauer Gmbh-Verlag Medizin Naturwissenschaften
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dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Cd40
dc.subject
Cd40l
dc.subject
Inflammation
dc.subject
Mac-1
dc.subject
Mice
dc.subject
Neointima Formation
dc.subject
Restenosis
dc.subject.classification
Medicina Critica y de Emergencia
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dc.subject.classification
Medicina Clínica
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dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD
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dc.title
Interruption of classic CD40L-CD40 signalling but not of the novel CD40L-Mac-1 interaction limits arterial neointima formation in mice
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2018-12-21T15:23:08Z
dc.journal.volume
112
dc.journal.number
2
dc.journal.pagination
379-389
dc.journal.pais
Alemania
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dc.journal.ciudad
Stuttgart
dc.description.fil
Fil: Willecke, Florian. University Of Freiburg; Alemania
dc.description.fil
Fil: Tiwari, Shilpa. University Of Freiburg; Alemania
dc.description.fil
Fil: Rupprecht, Benjamin. University Of Freiburg; Alemania
dc.description.fil
Fil: Wolf, Dennis. University Of Freiburg; Alemania
dc.description.fil
Fil: Hergeth, Sonja. University Of Freiburg; Alemania
dc.description.fil
Fil: Hoppe, Natalie. University Of Freiburg; Alemania
dc.description.fil
Fil: Dufner, Bianca. University Of Freiburg; Alemania
dc.description.fil
Fil: Schulte, Lisa. University Of Freiburg; Alemania
dc.description.fil
Fil: Anto Michel, Nathaly. University Of Freiburg; Alemania
dc.description.fil
Fil: Bukosza, Nora. University Of Freiburg; Alemania
dc.description.fil
Fil: Marchini, Timoteo Oscar. University Of Freiburg; Alemania. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina
dc.description.fil
Fil: Jäekel, Markus. University Of Freiburg; Alemania
dc.description.fil
Fil: Stachon, Peter. University Of Freiburg; Alemania
dc.description.fil
Fil: Hilgendorf, Ingo. University Of Freiburg; Alemania
dc.description.fil
Fil: Zeschky, Katharina. University Of Freiburg; Alemania
dc.description.fil
Fil: Schleicher, Rebecca. University Of Tübingen; Alemania
dc.description.fil
Fil: Langer, Harald. University Of Tübingen; Alemania
dc.description.fil
Fil: von zur Muhlen, Constantin. University Of Freiburg; Alemania
dc.description.fil
Fil: Bode, Christoph. University Of Freiburg; Alemania
dc.description.fil
Fil: Karlheinz, Peter. Baker Idi Heart And Diabetes Institute; Australia
dc.description.fil
Fil: Zirlik, Andreas. University Of Freiburg; Alemania
dc.journal.title
Thrombosis and Haemostasis
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dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1160/TH13-08-0653
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