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Cheng, I-Fen
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Cheng, I-Fen
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Cheng, I-Fen
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Cheng, I.-F.
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2014Journal Article [["dc.bibliographiccitation.firstpage","65"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Cellular Reprogramming"],["dc.bibliographiccitation.lastpage","76"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Streckfuss-Bömeke, Katrin"],["dc.contributor.author","Jende, Jörg"],["dc.contributor.author","Cheng, I-Fen"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Guan, Kaomei"],["dc.date.accessioned","2017-09-07T11:52:34Z"],["dc.date.available","2017-09-07T11:52:34Z"],["dc.date.issued","2014"],["dc.description.abstract","On the basis of their self-renewal capacity and their ability to differentiate into derivatives of all three germ layers, germ line–derived multipotent adult stem cells (maGSCs) from mouse testis might serve as one of preferable sources for pluripotent stem cells in regenerative medicine. In our study, we aimed for an efficient hepatic differentiation protocol that is applicable for both maGSCs and embryonic stem cells (ESCs). We attempted to accomplish this goal by using a new established co-culture system with OP9 stroma cells for direct differentiation of maGSCs and ESCs into hepatic cells. We found that the hepatic differentiation of maGSCs was induced by the OP9 co-culture system in comparison to the gelatin culture. Furthermore, we showed that the combination of OP9 co-culture with activin A resulted in the increased expression of endodermal and early hepatic markers Gata4, Sox17, Foxa2, Hnf4, Afp, and Ttr compared to differentiated cells on gelatin or on OP9 alone. Moreover, the hepatic progenitors were capable of differentiating further into mature hepatic cells, demonstrated by the expression of liver-specific markers Aat, Alb, Tdo2, Krt18, Krt8, Krt19, Cps1, Sek, Cyp7a1, Otc, and Pah. A high percentage of maGSC-derived hepatic progenitors (51% AFP- and 61% DLK1-positive) and mature hepatic-like cells (26% ALB-positive) were achieved using this OP9 co-culture system. These generated hepatic cells successfully demonstrated in vitro functions associated with mature hepatocytes, including albumin and urea secretion, glycogen storage, and uptake of low-density lipoprotein. The established co-culture system for maGSCs into functional hepatic cells might serve as a suitable model to delineate the differentiation process for the generation of high numbers of mature hepatocytes in humans without genetic manipulations and make germ line–derived stem cells a potential autologous and alternative cell source for hepatic transplants in metabolic liver disorders."],["dc.identifier.doi","10.1089/cell.2013.0057"],["dc.identifier.gro","3144969"],["dc.identifier.pmid","24380658"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2652"],["dc.language.iso","en"],["dc.notes.intern","Crossref Import"],["dc.notes.status","final"],["dc.relation.issn","2152-4971"],["dc.title","Efficient Generation of Hepatic Cells from Multipotent Adult Mouse Germ-Line Stem Cells Using an OP9 Co-Culture System"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]Details DOI PMID PMC2007Conference Abstract [["dc.bibliographiccitation.issue","16"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.volume","116"],["dc.contributor.author","Heida, Nana-Maria"],["dc.contributor.author","Schroeter, M. R."],["dc.contributor.author","Cheng, I-Fen"],["dc.contributor.author","Mueller, Jan-Peter"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Konstantindes, Stavros"],["dc.contributor.author","Schaefer, Katrin"],["dc.date.accessioned","2018-11-07T10:57:45Z"],["dc.date.available","2018-11-07T10:57:45Z"],["dc.date.issued","2007"],["dc.format.extent","839"],["dc.identifier.isi","000250394303788"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50323"],["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","Effects of obesity and weight loss on the functional 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"]]Details WOS2013Journal Article Research Paper [["dc.bibliographiccitation.firstpage","806"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Stem Cell Research"],["dc.bibliographiccitation.lastpage","819"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Dudek, Jan"],["dc.contributor.author","Cheng, I-Fen"],["dc.contributor.author","Balleininger, Martina"],["dc.contributor.author","Vaz, Frederic M."],["dc.contributor.author","Streckfuss-Bömeke, Katrin"],["dc.contributor.author","Hübscher, Daniela"],["dc.contributor.author","Vukotic, Milena"],["dc.contributor.author","Wanders, Ronald J. A."],["dc.contributor.author","Rehling, Peter"],["dc.contributor.author","Guan, Kaomei"],["dc.date.accessioned","2017-09-07T11:47:37Z"],["dc.date.available","2017-09-07T11:47:37Z"],["dc.date.issued","2013"],["dc.description.abstract","Barth syndrome (BTHS) patients carrying mutations in tafazzin (TAZ1), which is involved in the final maturation of cardiolipin, present with dilated cardiomyopathy, skeletal myopathy, growth retardation and neutropenia. To study how mitochondrial function is impaired in BTHS patients, we generated induced pluripotent stem cells (iPSCs) to develop a novel and relevant human model system for BTHS. BTHS-iPSCs generated from dermal fibroblasts of three patients with different mutations in TAZ1 expressed pluripotency markers, and were able to differentiate into cells derived from all three germ layers both in vitro and in vivo. We used these cells to study the impact of tafazzin deficiency on mitochondria( oxidative phosphorylation. We found an impaired remodeling of cardiolipin, a dramatic decrease in basal oxygen consumption rate and in the maximal respiratory capacity in BTHS-iPSCs. Simultaneous measurement of extra-cellular acidification rate allowed us a thorough assessment of the metabolic deficiency in BTHS patients. Blue native gel analyses revealed that decreased respiration coincided with dramatic structural changes in respiratory chain supercomplexes leading to a massive increase in generation of reactive oxygen species. Our data demonstrate that BTHS-iPSCs are capable of modeling BTHS by recapitulating the disease phenotype and thus are important tools for studying the disease mechanism. (C) 2013 The Authors. Published by Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.scr.2013.05.005"],["dc.identifier.gro","3142297"],["dc.identifier.isi","000323586600012"],["dc.identifier.pmid","23792436"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11333"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/6720"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/12"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A04: Patienten-spezifische induzierte pluripotente Stammzellen zur funktionellen Untersuchung von Ryanodinrezeptor-Mutationen"],["dc.relation","SFB 1002 | A06: Molekulare Grundlagen mitochondrialer Kardiomyopathien"],["dc.relation.issn","1873-5061"],["dc.relation.workinggroup","RG Guan (Application of patient-specific induced pluripotent stem cells in disease modelling)"],["dc.relation.workinggroup","RG Rehling (Mitochondrial Protein Biogenesis)"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Cardiolipin deficiency affects respiratory chain function and organization in an induced pluripotent stem cell model of Barth syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2012Journal Article Research Paper [["dc.bibliographiccitation.firstpage","207"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Vascular Research"],["dc.bibliographiccitation.lastpage","220"],["dc.bibliographiccitation.volume","49"],["dc.contributor.author","Cheng, I-Fen"],["dc.contributor.author","Kaiser, Diana"],["dc.contributor.author","Huebscher, Daniela"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Guan, Kaomei"],["dc.contributor.author","Schaefer, Katrin"],["dc.date.accessioned","2017-09-07T11:43:10Z"],["dc.date.available","2017-09-07T11:43:10Z"],["dc.date.issued","2012"],["dc.description.abstract","Pluripotent stem cells hold great promise for the treatment of cardiovascular disease. We previously described multipotent adult germline stem cells (maGSCs) from mouse testis with differentiation potential similar to embryonic stem cells. The aim of this work was to differentiate maGSCs into functional endothelial cells and to study their potential for vasculogenesis. MaGSCs were cocultivated with OP9 stromal cells to induce differentiation into cardiovascular progenitors, i.e. fetal liver kinase 1-positive (Flk-1(+)) cells. Five days later, Flk-1(+) cells were separated using fluorescence-activated cell sorting, followed by cultivation on collagen type IV under endothelial differentiation conditions. At different time points, maGSC-derived endothelial-like cells were characterized using RT-PCR, flow cytometry, immunofluorescence and functional assays. Cultivation of Flk-1(+) cells resulted in the progressive upregulation of endothelial cell markers, including VE-cadherin, von Willebrand factor and endothelial nitric oxide synthase. Moreover, Flk-1(+) maGSC-derived endothelial-like cells were able to branch and form networks in vitro and promoted functional blood vessel formation in vivo. Importantly, Flk-1(+) cells retained their potential to proliferate and could be continuously expanded, while the ability of contact inhibition was preserved. Thus, maGSCs may provide a useful source of endothelial-like cells to study the basic mechanisms of vasculogenesis or endothelial differentiation. Copyright 2012S. Karger AG, Basel"],["dc.identifier.doi","10.1159/000332910"],["dc.identifier.gro","3142600"],["dc.identifier.isi","000303967900003"],["dc.identifier.pmid","22433575"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9087"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1018-1172"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Differentiation of Multipotent Adult Germ line Stem Cells Derived from Mouse Testis into Functional Endothelial Cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2016Journal Article Research Paper [["dc.bibliographiccitation.firstpage","139"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","EMBO Molecular Medicine"],["dc.bibliographiccitation.lastpage","154"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Dudek, Jan"],["dc.contributor.author","Cheng, I-Fen"],["dc.contributor.author","Chowdhury, Arpita"],["dc.contributor.author","Wozny, Katharina"],["dc.contributor.author","Balleininger, Martina"],["dc.contributor.author","Reinhold, Robert"],["dc.contributor.author","Grunau, Silke"],["dc.contributor.author","Callegari, Sylvie"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Wanders, Ronald JA"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Brügger, Britta"],["dc.contributor.author","Guan, Kaomei"],["dc.contributor.author","Rehling, Peter"],["dc.date.accessioned","2017-09-07T11:53:31Z"],["dc.date.available","2017-09-07T11:53:31Z"],["dc.date.issued","2016"],["dc.description.abstract","Barth syndrome (BTHS) is a cardiomyopathy caused by the loss of tafazzin, a mitochondrial acyltransferase involved in the maturation of the glycerophospholipid cardiolipin. It has remained enigmatic as to why a systemic loss of cardiolipin leads to cardiomyopathy. Using a genetic ablation of tafazzin function in the BTHS mouse model, we identified severe structural changes in respiratory chain supercomplexes at a pre‐onset stage of the disease. This reorganization of supercomplexes was specific to cardiac tissue and could be recapitulated in cardiomyocytes derived from BTHS patients. Moreover, our analyses demonstrate a cardiac‐specific loss of succinate dehydrogenase (SDH), an enzyme linking the respiratory chain with the tricarboxylic acid cycle. As a similar defect of SDH is apparent in patient cell‐derived cardiomyocytes, we conclude that these defects represent a molecular basis for the cardiac pathology in Barth syndrome."],["dc.identifier.doi","10.15252/emmm.201505644"],["dc.identifier.fs","615879"],["dc.identifier.gro","3145083"],["dc.identifier.pmid","26697888"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13136"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2780"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/101"],["dc.language.iso","en"],["dc.notes.intern","Crossref Import"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A06: Molekulare Grundlagen mitochondrialer Kardiomyopathien"],["dc.relation.issn","1757-4676"],["dc.relation.issn","1757-4684"],["dc.relation.workinggroup","RG Guan (Application of patient-specific induced pluripotent stem cells in disease modelling)"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Rehling (Mitochondrial Protein Biogenesis)"],["dc.relation.workinggroup","RG Toischer (Kardiales Remodeling)"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject","Barth syndrome; Cardiolipin, Mitochondriar; Respiratory chain; Succinate dehydrogenase"],["dc.title","Cardiac-specific succinate dehydrogenase deficiency in Barth syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI PMID PMC2010Journal Article Research Paper [["dc.bibliographiccitation.firstpage","357"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of the American College of Cardiology"],["dc.bibliographiccitation.lastpage","367"],["dc.bibliographiccitation.volume","55"],["dc.contributor.author","Heida, Nana-Maria"],["dc.contributor.author","Mueller, Jan-Peter"],["dc.contributor.author","Cheng, I-Fen"],["dc.contributor.author","Leifheit-Nestler, Maren"],["dc.contributor.author","Faustin, Vivien"],["dc.contributor.author","Riggert, Joachim"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Konstantinides, Stavros"],["dc.contributor.author","Schaefer, Katrin"],["dc.date.accessioned","2017-09-07T11:46:10Z"],["dc.date.available","2017-09-07T11:46:10Z"],["dc.date.issued","2010"],["dc.description.abstract","Objectives The purpose of this study was to examine the impact of obesity and weight loss on the angiogenic and regenerative capacity of endothelial progenitor cells (EPCs). Background EPCs participate in angiogenesis and tissue repair. Several cardiovascular risk factors are associated with EPC dysfunction. Methods Early outgrowth EPCs were isolated from 49 obese (age 42 +/- 14 years; body mass index 42 +/- 7 kg/m(2)) normo-glycemic participants in a professional weight reduction program and compared with those from 49 age-matched lean controls. EPC function was tested both in vitro and in vivo. Results EPCs expanded from the obese possessed reduced adhesive, migratory, and angiogenic capacity, and mice treated with obese EPCs exhibited reduced EPC homing in ischemic hind limbs in vivo. EPCs from the obese subjects failed to respond to conditioned medium of lean controls or to potent angiogenic factors such as vascular endothelial growth factor. Although no differences existed between lean and obese EPCs regarding the surface expression of vascular endothelial growth factor or chemokine receptors, basal p38 mitogen-activated protein kinase (MAPK) phosphorylation was elevated in obese EPCs (3.7 +/- 2.1-fold increase; p = 0.006). These cells also showed reduced secretion of the angiogenic chemokines interleukin-8 (p = 0.047) and monocyte chemoattractant protein-1 (p = 0.012). By inhibiting p38 MAPK, we could restore chemokine levels to those of lean control EPCs and also improve the angiogenic properties of obese EPCs. Accordingly, 6-month follow-up of 26 obese persons who achieved significant weight reduction revealed normalization of p38 MAPK phosphorylation levels and improved EPC function. Conclusions Obesity is associated with a reversible functional impairment of EPCs. This involves reduced secretion of angiogenic chemokines and increased basal phosphorylation of signaling molecules, notably p38 MAPK. (J Am Coll Cardiol 2010; 55: 357-67) (C) 2010 by the American College of Cardiology Foundation"],["dc.identifier.doi","10.1016/j.jacc.2009.09.031"],["dc.identifier.gro","3142979"],["dc.identifier.isi","000273802200013"],["dc.identifier.pmid","20117442"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6292"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/442"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","0735-1097"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Effects of Obesity and Weight Loss on the Functional Properties of Early Outgrowth Endothelial Progenitor Cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2010Journal Article Research Paper [["dc.bibliographiccitation.firstpage","200"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Arteriosclerosis, Thrombosis, and Vascular Biology"],["dc.bibliographiccitation.lastpage","206"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Heida, Nana-Maria"],["dc.contributor.author","Leifheit-Nestler, Maren"],["dc.contributor.author","Schroeter, Marco R."],["dc.contributor.author","Mueller, Jan-Peter"],["dc.contributor.author","Cheng, I-Fen"],["dc.contributor.author","Henkel, Sarah"],["dc.contributor.author","Limbourg, Anne"],["dc.contributor.author","Limbourg, Florian P."],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Quigley, James P."],["dc.contributor.author","Ruggeri, Zaverio M."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Konstantinides, Stavros"],["dc.contributor.author","Schaefer, Katrin"],["dc.date.accessioned","2017-09-07T11:46:10Z"],["dc.date.available","2017-09-07T11:46:10Z"],["dc.date.issued","2010"],["dc.description.abstract","Objective-To investigate the capacity of the adipokine leptin to promote angiogenesis by modulating the function of circulating angiogenic cells (CACs). Methods and Results-In vitro, leptin specifically promoted CAC adhesion to tubular endothelial structures and migration along outgrowing sprouts of endothelial cells. In vivo, stimulation of CACs with leptin increased their capacity to promote new vessel formation in the chorioallantoic membrane of chicken embryos and to improve neovascularization of ischemic murine hind limbs. These effects required the phosphorylation of alpha v beta 5 integrins, which depended on the interaction of leptin with its receptor ObR, and on Janus kinase (JAK) 2- and phospholipase C (PLC) gamma-mediated activation of Src kinase. Protein tyrosine phosphatase 1B, a negative regulator of leptin signaling, was overexpressed in CACs from obese, hyperleptinemic individuals, and this was associated with insensitivity of CACs to the angiogenic effects of leptin. Weight loss (by 30 +/- 15 kg) normalized protein tyrosine phosphatase 1B expression in CACs and restored their responsiveness to leptin. A similar dose- dependent response was found after incubation of CACs from obese subjects with a protein tyrosine phosphatase 1B inhibitor ex vivo. Conclusion-Our results point to the ObR-Src kinase-alpha v beta 5 cross talk as a distinct novel component of the network of specific interactions between integrins and cytokine receptors in angiogenesis. (Arterioscler Thromb Vasc Biol. 2010; 30: 200-206.)"],["dc.identifier.doi","10.1161/ATVBAHA.109.192807"],["dc.identifier.gro","3142969"],["dc.identifier.isi","000273799900014"],["dc.identifier.pmid","19910644"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/431"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: National Institutes of Health [NIH HL-75736]"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1079-5642"],["dc.title","Leptin Enhances the Potency of Circulating Angiogenic Cells Via Src Kinase and Integrin alpha v beta 5 Implications for Angiogenesis in Human Obesity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2007Conference Abstract [["dc.bibliographiccitation.issue","16"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.volume","116"],["dc.contributor.author","Heida, Nana-Maria"],["dc.contributor.author","Schroeter, M. R."],["dc.contributor.author","Cheng, I-Fen"],["dc.contributor.author","Deryugina, Elena I."],["dc.contributor.author","Korff, Thomas"],["dc.contributor.author","Quigley, James P."],["dc.contributor.author","Ruggeri, Zaverio M."],["dc.contributor.author","Mueller, Jan-Peter"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Konstantmides, Stavros"],["dc.contributor.author","Schaefer, Katrin"],["dc.date.accessioned","2018-11-07T10:57:41Z"],["dc.date.available","2018-11-07T10:57:41Z"],["dc.date.issued","2007"],["dc.format.extent","175"],["dc.identifier.isi","000250394300776"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50313"],["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 potentiates the angiogenic properties of endothelial progenitor cells in vitro and in vivo"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details WOS2010Conference Abstract [["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"]]Details WOS2008Conference Abstract [["dc.bibliographiccitation.issue","18"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.volume","118"],["dc.contributor.author","Heida, Nana-Maria"],["dc.contributor.author","Mueller, Jan-Peter"],["dc.contributor.author","Cheng, I-Fen"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Konstantinides, Stavros V."],["dc.contributor.author","Schaefer, Katrin"],["dc.date.accessioned","2018-11-07T11:09:53Z"],["dc.date.available","2018-11-07T11:09:53Z"],["dc.date.issued","2008"],["dc.format.extent","S509"],["dc.identifier.isi","000262104501258"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53098"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","81st Annual Scientific Session of the American-Heart-Association"],["dc.relation.eventlocation","New Orleans, LA"],["dc.relation.issn","0009-7322"],["dc.title","Mechanisms Mediating The Proangiogenic Effects Of Leptin On Endothelial Progenitor Cells From Lean And Obese Individuals"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details WOS