Schroeter, Marco Robin

[["dc.bibliographiccitation.issue","18"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.volume","120"],["dc.contributor.author","Leifheit, Maren"],["dc.contributor.author","Conrad, Gaby"],["dc.contributor.author","Heide, Nana-Maria"],["dc.contributor.author","Schroeter, Marco"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Konstantinides, Stavros V."],["dc.contributor.author","Schaefer, Katrin"],["dc.date.accessioned","2018-11-07T11:22:15Z"],["dc.date.available","2018-11-07T11:22:15Z"],["dc.date.issued","2009"],["dc.format.extent","S1151"],["dc.identifier.isi","000271831504246"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55953"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","82nd Scientific Session of the American-Heart-Association"],["dc.relation.eventlocation","Orlando, FL"],["dc.relation.issn","0009-7322"],["dc.title","Overexpression of Integrin Beta5 Enhances the Paracrine Angiogenic Properties of Early Outgrowth Endothelial Progenitor Cells via Sire Kinase-Mediated Activation of STAT3"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1254"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Arteriosclerosis, Thrombosis, and Vascular Biology"],["dc.bibliographiccitation.lastpage","1259"],["dc.bibliographiccitation.volume","26"],["dc.contributor.author","Schäfer, Katrin"],["dc.contributor.author","Schroeter, Marco R."],["dc.contributor.author","Dellas, Claudia"],["dc.contributor.author","Puls, Miriam"],["dc.contributor.author","Nitsche, Mirko"],["dc.contributor.author","Weiss, Elisabeth"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Konstantinides, Stavros V."],["dc.date.accessioned","2017-09-07T11:52:41Z"],["dc.date.available","2017-09-07T11:52:41Z"],["dc.date.issued","2006"],["dc.description.abstract","Objective - To investigate the ability of bone marrow ( BM) - derived cells to modulate neointimal growth after injury by expressing plasminogen activator inhibitor-1 ( PAI-1). Methods and Results - We performed BM transplantation ( BMT) in lethally irradiated wild- type ( WT) and PAI-1-/- mice. Three weeks after carotid injury with ferric chloride, analysis of Y-chromosome DNA expression in the vessel wall of female hosts revealed that 20.8 +/- 6.0% of the cells in the neointima and 37.6 +/- 5.7% of those in the media were of BM origin. Lack of PAI-1 in either the host or the donor cells did not affect recruitment of BM-derived cells into sites of vascular injury. The neointima consisted predominantly of smooth muscle cells, and a proportion of these cells expressed PAI-1. Overall, lack of PAI-1 was associated with enhanced neointimal formation. However, importantly, BMTWT -> PAI-1-/- mice exhibited reduced neointimal area ( P = 0.05) and luminal stenosis ( P = 0.04) compared with BMTPAI-1-/--> PAI-1-/- mice. Although PAI-1-expressing cells were shown to be present in BMTWT -> PAI-1-/- lesions, these mice did not exhibit detectable levels of the inhibitor in the circulation, suggesting that local production of PAI-1 by cells in the neointima and media was sufficient to reduce luminal stenosis. Conclusions - PAI-1 from BM-derived cells appears capable of suppressing neointimal growth after vascular injury."],["dc.identifier.doi","10.1161/01.ATV.0000215982.14003.b7"],["dc.identifier.gro","3143681"],["dc.identifier.isi","000237644000012"],["dc.identifier.pmid","16514083"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1221"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1079-5642"],["dc.title","Plasminogen Activator Inhibitor-1 From Bone Marrow–Derived Cells Suppresses Neointimal Formation After Vascular Injury in Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","63"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Atherosclerosis"],["dc.bibliographiccitation.lastpage","73"],["dc.bibliographiccitation.volume","205"],["dc.contributor.author","Schroeter, M. R."],["dc.contributor.author","Humboldt, Tim"],["dc.contributor.author","Schaefer, Katrin"],["dc.contributor.author","Konstantinides, Stavros V."],["dc.date.accessioned","2018-11-07T08:27:59Z"],["dc.date.available","2018-11-07T08:27:59Z"],["dc.date.issued","2009"],["dc.description.abstract","Statins enhance incorporation of bone marrow-derived cells into experimental neointimal lesions. However, the contribution of progenitor cells to progression of spontaneous atherosclerotic plaques, and the possible modulatory role of statins in this process, remain poorly understood. We compared the effects of rosuvastatin (1 and 10 mg/kg BW) and pravastatin (10 mg/kg) on progenitor cell mobilisation, recruitment into atherosclerotic plaques, and lesion growth. Statins were administered over 8 weeks to apolipoprotein E knockout mice on atherogenic diet. In addition, mice were lethally irradiated, followed by transplantation of bone marrow from LacZ transgenic mice. Rosuvastatin reduced lesion area and intima-to-media ratio at the brachiocephalic artery compared to vehicle. while both parameters were not significantly altered by pravastatin. Rosuvastatin also augmented endothelialisation (P<0.05) and reduced the smooth muscle cells (SMC) content (P= 0.042) of lesions. Numbers of c-kit, sca-1 and flk-1, sca-1 double-positive progenitor cells were significantly increased in rosuvastatin compared to controltreated mice, both in the bone marrow and the peripheral blood. Similarly, the number of spleen-derived acLDL, lectin double-positive progenitor cells (P= 0.001) and colony-forming units (P= 0.0104) was significantly increased in mice treated with rosuvastatin compared to vehicle alone. In the bone marrow, increased Akt and p42/44 MAP kinase phosphorylation and upregulated SDF1 alpha mRNA expression were observed. Importantly, rosuvastatin treatment also increased the plasma levels of c-kit ligand (P = 0.003), and the number of c-kit-positive cells within atherosclerotic lesions (P = 0.041). Our findings suggest that rosuvastatin reduces the size of atherosclerotic plaques, and this effect appears to involve progenitor cell mobilisation and recruitment into vascular lesions. (C) 2008 Elsevier Ireland Ltd. All rights reserved."],["dc.description.sponsorship","University of Goettingen; Astra Zeneca Ltd"],["dc.identifier.doi","10.1016/j.atherosclerosis.2008.11.013"],["dc.identifier.isi","000268115000011"],["dc.identifier.pmid","19111832"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16320"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Ireland Ltd"],["dc.relation.issn","0021-9150"],["dc.title","Rosuvastatin reduces atherosclerotic lesions and promotes progenitor cell mobilisation and recruitment in apolipoprotein E knockout mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","323"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Histochemistry and Cell Biology"],["dc.bibliographiccitation.lastpage","333"],["dc.bibliographiccitation.volume","128"],["dc.contributor.author","Schroeter, M. R."],["dc.contributor.author","Schneiderman, Jacob"],["dc.contributor.author","Schumann, Bettina"],["dc.contributor.author","Glueckermann, Roland"],["dc.contributor.author","Grimmas, Petros"],["dc.contributor.author","Buchwald, Arnd B."],["dc.contributor.author","Tirilomis, Theodor"],["dc.contributor.author","Schoendube, Friedrich Albert"],["dc.contributor.author","Konstantinides, Stavros V."],["dc.contributor.author","Schaefer, Katrin"],["dc.date.accessioned","2018-11-07T10:58:06Z"],["dc.date.available","2018-11-07T10:58:06Z"],["dc.date.issued","2007"],["dc.description.abstract","Clinical and experimental evidence suggests that the adipokine leptin may be important for the development of cardiovascular complications associated with obesity, possibly through interaction with its receptor on vascular cells. In the present study, we systematically analysed expression of the leptin receptor in normal and diseased vascular specimens using immunohistochemistry, immunofluorescence and quantitative real time-PCR. In particular, human atherosclerotic plaques as well as experimental vascular lesions induced in hypercholesterolemic mice and minipigs, respectively, were examined. Our results demonstrate the presence of the leptin receptor in normal vessel wall segments as well as neointimal or atherosclerotic lesions. In the latter, ObR expressing cells were predominantly localised on the luminal border and within the subintima, and coexpression of von Willebrand factor, VEGF receptor-2 or VE cadherin identified them as endothelial cells. Moreover, CD14-positive monocytes/macrophages were strongly positive for the leptin receptor. In contrast, only few ObR-expressing smooth muscle cells could be detected in human atherosclerotic plaques. The findings of the present study thus support a possible action of leptin on the cardiovascular system by demonstrating expression of the leptin receptor in different types of vascular lesions."],["dc.identifier.doi","10.1007/s00418-007-0319-1"],["dc.identifier.isi","000249523100005"],["dc.identifier.pmid","17680264"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50402"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0948-6143"],["dc.title","Expression of the leptin receptor in different types of vascular lesions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1146"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Journal of Vascular Surgery"],["dc.bibliographiccitation.lastpage","1155"],["dc.bibliographiccitation.volume","48"],["dc.contributor.author","Schneiderman, Jacob"],["dc.contributor.author","Simon, Amos J."],["dc.contributor.author","Schroeter, M. R."],["dc.contributor.author","Flugelman, Moshe Y."],["dc.contributor.author","Konstantinides, Stavros V."],["dc.contributor.author","Schaefer, Katrin"],["dc.date.accessioned","2018-11-07T11:09:36Z"],["dc.date.available","2018-11-07T11:09:36Z"],["dc.date.issued","2008"],["dc.description.abstract","Background. Carotid artery lesions from symptomatic patients are characterized by inflammation and neovascularization. The adipokine leptin promotes angiogenesis and activates inflammatory cells, and the leptin receptor (ob gene-encoded receptor), ObR, is expressed in advanced atherosclerotic lesions. The present study quantitatively analyzed ObR messenger RNA (mRNA) expression and immunoreactivity in carotid artery plaques from symptomatic and asymptomatic persons. Plaque angiogenesis, gene expression of vascular endothelial growth factor (VEGF), and macrophage density were also analyzed. Methods: Carotid endarterectomy specimens were collected from 26 patients undergoing surgery for hemispheric cerebrovascular symptoms (n = 13) or progressive asymptomatic internal carotid stenosis (n = 13). A representative sample, including part of the most active site, was collected from each lesion and evaluated by real-time polymerase chain reaction analysis for ObR(long) and ObR(common) isoforms, VEGF(165), and macrophage adhesion molecule-1 (Mac-1) mRNA, and by immunohistochemistry for ObR, von Willebrand factor (vWF), and CD68 antigen expression. Results: All plaques exhibited advanced atherosclerosis (American Heart Association class IV through VI). Transcript levels were preferentially elevated in symptomatic plaques for ObR(long) (P = .0006) and ObR(common) (P = .033), with a simultaneous upregulation of V-EGF(165) (P = .001) and Mac-1 mRNA expression (P = .003). Immunohistochemical analysis confirmed a significant increase of ObR antigen levels (P = .011) and CD68-positive inflammatory cells (P = .049) in symptomatic plaques, whereas neovascularization, evident in all plaques, was similar in both groups (P = .7). Conclusion: The ObR(long) and ObR(common) genes are upregulated and their protein preferentially synthesized in clinically symptomatic carotid plaques. Moreover, ObR expression is positively correlated with augmentation of gene transcripts related to macrophage density and neovascularization. These data suggest that ObR(long) and ObR(common) may be linked with histologic features of carotid plaque instability, which are associated with cerebral ischemic symptoms. (J Vasc Surg 2008;48:1146-55.)"],["dc.identifier.doi","10.1016/j.jvs.2008.06.054"],["dc.identifier.isi","000260725300012"],["dc.identifier.pmid","18829234"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53043"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Mosby-elsevier"],["dc.relation.issn","0741-5214"],["dc.title","Leptin receptor is elevated in carotid plaques from neurologically symptomatic patients and positively correlated with augmented macrophage density"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","21"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.volume","122"],["dc.contributor.author","Schroeter, M. R."],["dc.contributor.author","Stein, Susanne"],["dc.contributor.author","Heida, Nana-Maria"],["dc.contributor.author","Leifheit-Nestler, Maren"],["dc.contributor.author","Christiansen, Hans"],["dc.contributor.author","Cheng, I-Fen"],["dc.contributor.author","Shah, Ajay M."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Konstantinides, Stavros V."],["dc.contributor.author","Schaefer, Katrin"],["dc.date.accessioned","2018-11-07T08:36:40Z"],["dc.date.available","2018-11-07T08:36:40Z"],["dc.date.issued","2010"],["dc.identifier.isi","000208231600521"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18371"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.issn","0009-7322"],["dc.title","Leptin Promotes the Mobilization of Fetal Liver Kinase 1-Positive Vascular Progenitor Cells From the Bone Marrow in a NOX2/MMP9-dependent Manner and Enhances Neovascularization after Ischemia"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","18"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.volume","114"],["dc.contributor.author","Puls, Miriam"],["dc.contributor.author","Schroeter, Marco"],["dc.contributor.author","Steier, Jasmin"],["dc.contributor.author","Stijohann, Lena"],["dc.contributor.author","Andreas, Stefan"],["dc.contributor.author","Raupach, Tobias"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Konstantinides, Stavros V."],["dc.contributor.author","Schaefer, Katrin"],["dc.date.accessioned","2018-11-07T09:05:35Z"],["dc.date.available","2018-11-07T09:05:35Z"],["dc.date.issued","2006"],["dc.format.extent","856"],["dc.identifier.isi","000241792805455"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25357"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.eventlocation","Chicago, IL"],["dc.relation.issn","0009-7322"],["dc.title","Effect of smoking cessation on the number, proliferation and adhesive properties of endothelial progenitor cells"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","980"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Arteriosclerosis Thrombosis and Vascular Biology"],["dc.bibliographiccitation.lastpage","U279"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Schroeter, M. R."],["dc.contributor.author","Eschholz, Norman"],["dc.contributor.author","Herzberg, Sebastian"],["dc.contributor.author","Jerchel, Isabel"],["dc.contributor.author","Leifheit-Nestler, Maren"],["dc.contributor.author","Czepluch, Frauke S."],["dc.contributor.author","Chalikias, Georgios"],["dc.contributor.author","Konstantinides, Stavros V."],["dc.contributor.author","Schaefer, Katrin"],["dc.date.accessioned","2018-11-07T09:25:35Z"],["dc.date.available","2018-11-07T09:25:35Z"],["dc.date.issued","2013"],["dc.description.abstract","Objective-Clinical and experimental evidence suggests that periadventitial adipose tissue may modulate vascular lesion formation. The aim of this study was to determine the role of perivascular leptin expression on neointima formation and to differentiate it from local inflammation and systemically elevated leptin levels. Approach and Results-Increased neointima formation after carotid artery injury was observed in hyperleptinemic, diet-induced obese wild-type mice, but not in leptin-deficient ob/ob mice. High-fat diet was associated with increased leptin expression in visceral adipose tissue (VAT) as well as in perivascular adipose tissue. Perivascular leptin overexpression achieved by adenoviral vectors enhanced intimal cell proliferation and neointima formation in wild-type mice, but not in leptin receptor-deficient mice. Perivascular transplantation of VAT from high-fat diet-induced obese wild-type mice around the carotid artery of immunodeficient mice also promoted neointima formation, without affecting body weight or systemic leptin levels, and this effect was absent, if VAT from ob/ob mice was used. On the contrary, perivascular transplantation of VAT from ob/ob mice fed high-fat diet, characterized by marked immune cell accumulation, promoted neointimal hyperplasia also in the absence of leptin. In vitro, recombinant leptin and VAT-conditioned medium increased human arterial smooth muscle cell proliferation in a (partly) leptin-dependent manner. Conclusions-Our findings suggest that locally elevated leptin levels may promote neointima formation, independent of obesity and systemic hyperleptinemia, but also underline the importance of perivascular inflammation in mediating the increased cardiovascular risk in obesity. (Arterioscler Thromb Vasc Biol. 2013; 33: 980-987.)"],["dc.identifier.doi","10.1161/ATVBAHA.113.301393"],["dc.identifier.isi","000317476000019"],["dc.identifier.pmid","23520165"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30097"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","1079-5642"],["dc.title","Leptin-Dependent and Leptin-Independent Paracrine Effects of Perivascular Adipose Tissue on Neointima Formation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","18"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.volume","114"],["dc.contributor.author","Schroeter, Marco"],["dc.contributor.author","Sudholt, Philipp"],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Rafail, Stavros"],["dc.contributor.author","Dellas, Claudia"],["dc.contributor.author","Puls, Miriam"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Konstantinides, Stavros V."],["dc.contributor.author","Schaefer, Katrin"],["dc.date.accessioned","2018-11-07T09:05:23Z"],["dc.date.available","2018-11-07T09:05:23Z"],["dc.date.issued","2006"],["dc.format.extent","121"],["dc.identifier.isi","000241792800576"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25302"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.eventlocation","Chicago, IL"],["dc.relation.issn","0009-7322"],["dc.title","The adipokine leptin promotes integrin-mediated adhesion of endothelial progenitor cells"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","16"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.volume","116"],["dc.contributor.author","Schneiderman, Jacob"],["dc.contributor.author","Simon, Amos J."],["dc.contributor.author","Schroeter, M. R."],["dc.contributor.author","Engelberg, Isaac"],["dc.contributor.author","Flugelman, Moshe Y."],["dc.contributor.author","Konstantinides, Stavros V."],["dc.contributor.author","Shaefer, Katrin"],["dc.date.accessioned","2018-11-07T10:57:40Z"],["dc.date.available","2018-11-07T10:57:40Z"],["dc.date.issued","2007"],["dc.format.extent","107"],["dc.identifier.isi","000250394300473"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50308"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","80th Annual Scientific Session of the American-Heart-Association"],["dc.relation.eventlocation","Orlando, FL"],["dc.relation.issn","0009-7322"],["dc.title","Leptin receptor long isoform is increased and positively correlated with augmented macrophage infiltration and plaque neovascularization in carotid plaques from neurologically symptomatic patients"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]