Schroeter, Marco Robin

[["dc.bibliographiccitation.firstpage","480"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Vascular Research"],["dc.bibliographiccitation.lastpage","492"],["dc.bibliographiccitation.volume","45"],["dc.contributor.author","Schroeter, M. R."],["dc.contributor.author","Sawalich, Matthias"],["dc.contributor.author","Humboldt, Tim"],["dc.contributor.author","Leifheit, Maren"],["dc.contributor.author","Meurrens, Kris"],["dc.contributor.author","Berges, A. N."],["dc.contributor.author","Xu, H."],["dc.contributor.author","Lebrun, Stefan"],["dc.contributor.author","Wallerath, Thomas"],["dc.contributor.author","Konstantinides, Stavros V."],["dc.contributor.author","Schleef, Raymond"],["dc.contributor.author","Schaefer, Katrin"],["dc.date.accessioned","2018-11-07T11:20:17Z"],["dc.date.available","2018-11-07T11:20:17Z"],["dc.date.issued","2008"],["dc.description.abstract","Background: Cigarette smoking is a major risk factor for the development of cardiovascular disease. However, in terms of the vessel wall, the underlying pathomechanisms of cigarette smoking are incompletely understood, partly due to a lack of adequate in vivo models. Methods: Apolipoprotein E-deficient mice were exposed to filtered air (sham) or to cigarette mainstream smoke at a total particulate matter (TPM) concentration of 600 mu g/l for 1, 2, 3, or 4 h, for 5 days/week. After exposure for 10 8 1 weeks, arterial thrombosis and neointima formation at the carotid artery were induced using 10% ferric chloride. Results: Mice exposed to mainstream smoke exhibited shortened time to thrombotic occlusion (p < 0.01) and lower vascular patency rates (p < 0.001). Morphometric and immunohistochemical analysis of neointimal lesions demonstrated that mainstream smoke exposure increased the amount of alpha-actin-positive smooth muscle cells (p < 0.05) and dose-dependently increased the intima-to-media ratio (p < 0.05). Additional analysis of smooth muscle cells in vitro suggested that 10 mu g TPM/ml increased cell proliferation without affecting viability or apoptosis, whereas higher concentrations (100 and 500 mu g TPM/ml) appeared to be cytotoxic. Conclusions: Taken together, these findings suggest that cigarette smoking promotes arterial thrombosis and modulates the size and composition of neointimal lesions after arterial injury in apolipoprotein E-deficient mice. Copyright (C) 2008 S. Karger AG, Basel."],["dc.identifier.doi","10.1159/000127439"],["dc.identifier.isi","000260238700003"],["dc.identifier.pmid","18434747"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9356"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55500"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","1423-0135"],["dc.relation.issn","1018-1172"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Cigarette Smoke Exposure Promotes Arterial Thrombosis and Vessel Remodeling after Vascular Injury in Apolipoprotein E-Deficient Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]