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Role of endogenous Fas (CD95/Apo-1) ligand in balloon-induced apoptosis, inflammation, and neointima formation

Role of endogenous Fas (CD95/Apo-1) ligand in balloon-induced apoptosis, inflammation, and neointima formation

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Prüfsumme: MD5:9ea560af774d37c60d711e7512547d05

MATTER, Christian, Christos CHADJICHRISTOS, Patricia MEIER, Tobias von LUKOWICZ, Christine LOHMANN, Pia SCHULER, Dongming ZHANG, Bernhard ODERMATT, Eugen HOFMANN, Thomas BRUNNER, Brenda KWAK, Thomas LÜSCHER, 2006. Role of endogenous Fas (CD95/Apo-1) ligand in balloon-induced apoptosis, inflammation, and neointima formation. In: Circulation. 113(15), pp. 1879-1887. ISSN 0009-7322. eISSN 1524-4539. Available under: doi: 10.1161/CIRCULATIONAHA.106.611731

@article{Matter2006-04-18endog-14280, title={Role of endogenous Fas (CD95/Apo-1) ligand in balloon-induced apoptosis, inflammation, and neointima formation}, year={2006}, doi={10.1161/CIRCULATIONAHA.106.611731}, number={15}, volume={113}, issn={0009-7322}, journal={Circulation}, pages={1879--1887}, author={Matter, Christian and Chadjichristos, Christos and Meier, Patricia and Lukowicz, Tobias von and Lohmann, Christine and Schuler, Pia and Zhang, Dongming and Odermatt, Bernhard and Hofmann, Eugen and Brunner, Thomas and Kwak, Brenda and Lüscher, Thomas} }

Lohmann, Christine Hofmann, Eugen Lüscher, Thomas Lohmann, Christine Role of endogenous Fas (CD95/Apo-1) ligand in balloon-induced apoptosis, inflammation, and neointima formation Zhang, Dongming Brunner, Thomas Matter, Christian Schuler, Pia Odermatt, Bernhard Lüscher, Thomas deposit-license Chadjichristos, Christos First publ. in: Circulation ; 113 (2006), 15. - pp. 1879-1887 Background: Fas (CD95/Apo-1) ligand (FasL)–induced apoptosis in Fas-bearing cells is critically involved in modulating immune reactions and tissue repair. Apoptosis has also been described after mechanical vascular injury such as percutaneous coronary intervention. However, the relevance of cell death in this context of vascular repair remains unknown.<br />Methods and Results: To determine whether FasL-induced apoptosis is causally related to neointimal lesion formation, we subjected FasL-deficient (generalized lymphoproliferative disorder [gld], C57BL/6J) and corresponding wild-type (WT) mice to carotid balloon distension injury, which induces marked endothelial denudation and medial cell death. FasL expression in WT mice was induced in injured vessels compared with untreated arteries (P<0.05; n=5). Conversely, absence of functional FasL in gld mice decreased medial and intimal apoptosis (terminal deoxynucleotidyltransferase–mediated dUTP nick end labeling [TUNEL] index) at 1 hour and 7 days after balloon injury (P<0.05; n=6). In addition, peritoneal macrophages isolated from gld mice showed no apoptosis and enhanced migration (P<0.05; n=4). In parallel, we observed increased balloon-induced macrophage infiltrations (anti-CD68) in injured arteries of FasL-deficient animals (P<0.05; n=6). Together with enhanced proliferation (bromodeoxyuridine index; P<0.05), these events resulted in a further increase in medial and neointimal cells (P<0.01; n=8) with thickened neointima in gld mice (intima/media ratio, ×3.8 of WT; P<0.01).<br />Conclusions: Our data identify proapoptotic and antiinflammatory effects of endogenous FasL as important factors in the process of neointimal lesion formation after balloon injury. Moreover, they suggest that activation of FasL may decrease neointimal thickening after percutaneous coronary intervention. Chadjichristos, Christos Kwak, Brenda Kwak, Brenda 2011-10-20T09:37:12Z Lukowicz, Tobias von Brunner, Thomas Matter, Christian Odermatt, Bernhard Schuler, Pia eng Hofmann, Eugen Zhang, Dongming Lukowicz, Tobias von Meier, Patricia 2011-10-20T09:37:12Z Meier, Patricia 2006-04-18

Dateiabrufe seit 01.10.2014 (Informationen über die Zugriffsstatistik)

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