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Czepluch, Frauke S.
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Czepluch, Frauke S.
Official Name
Czepluch, Frauke S.
Alternative Name
Czepluch, F. S.
Czepluch, Frauke
Czepluch, F.
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2015Journal Article Research Paper [["dc.bibliographiccitation.firstpage","700"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Microcirculation"],["dc.bibliographiccitation.lastpage","710"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Czepluch, Frauke S."],["dc.contributor.author","Vogler, Melanie"],["dc.contributor.author","Kuschicke, Hendrik"],["dc.contributor.author","Meier, Julia"],["dc.contributor.author","Gogiraju, Rajinikanth"],["dc.contributor.author","Katschinski, Dörthe M."],["dc.contributor.author","Riggert, Joachim"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Schaefer, Katrin"],["dc.date.accessioned","2017-09-07T11:43:27Z"],["dc.date.available","2017-09-07T11:43:27Z"],["dc.date.issued","2015"],["dc.description.abstract","Objective: The zinc finger transcription factor KLF4 is known to control diverse EC functions. Methods: The functional role of KLF4 for angiogenesis and its association with CAD was examined in HUVECs and human CECs. Results: In two different angiogenesis assays, siRNA-mediated KLF4 downregulation impaired HUVEC sprouting and network formation. Conversely, KLF4 overexpression increased HUVEC sprouting and network formation. Similar findings were observed after incubation of HUVECs with CdM from KLF4 cDNA-transfected cells, suggesting a role of paracrine factors for mediating angiogenic KLF4 effects. In this regard, VEGF expression was increased in KLF4-overexpressing HUVECs, whereas its expression was reduced in HUVECs transfected with KLF4 siRNA. To examine the relevance of our in vitro findings for human endothelial dysfunction, we analyzed the expression of KLF4 in CECs of patients with stable CAD. Flow cytometry analyses revealed decreased numbers of KLF4-positive CECs in peripheral blood from CAD patients compared to healthy controls. Conclusions: Our findings suggest that KLF4 may represent a potential biomarker for EC dysfunction. In the future, (therapeutic) modulation of KLF4 may be useful in regulating EC function during vascular disease processes."],["dc.identifier.doi","10.1111/micc.12226"],["dc.identifier.gro","3141793"],["dc.identifier.isi","000365387200003"],["dc.identifier.pmid","26214161"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1135"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1549-8719"],["dc.relation.issn","1073-9688"],["dc.title","Circulating Endothelial Cells Expressing the Angiogenic Transcription Factor Kruppel-Like Factor 4 are Decreased in Patients with Coronary Artery Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2014Journal Article Research Paper [["dc.bibliographiccitation.firstpage","144"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Internal Medicine"],["dc.bibliographiccitation.lastpage","154"],["dc.bibliographiccitation.volume","275"],["dc.contributor.author","Czepluch, Frauke S."],["dc.contributor.author","Kuschicke, Hendrik"],["dc.contributor.author","Dellas, Claudia"],["dc.contributor.author","Riggert, Joachim"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Schaefer, Katrin"],["dc.date.accessioned","2017-09-07T11:46:53Z"],["dc.date.available","2017-09-07T11:46:53Z"],["dc.date.issued","2014"],["dc.description.abstract","BackgroundMonocytes and platelets are important cellular mediators of atherosclerosis. Human monocytes can be divided into CD14(++)CD16(-), CD14(++)CD16(+) and CD14(+)CD16(++) cells, which differ in their functional properties. The aim of this study was to examine monocyte subset distribution, monocyte-platelet aggregate (MPA) formation and expression of CCR5, the receptor of the platelet-derived chemokine CCL5, and to determine whether these parameters are altered in individuals with coronary atherosclerosis. MethodsPeripheral blood cells from 64 healthy blood donors (HBDs) and 60 patients with stable coronary artery disease (CAD) were stained with antibodies against CD14, CD16, CD42b and CCR5 and analysed by flow cytometry. Circulating CCL5 levels were determined using an enzyme-linked immunosorbent assay. ResultsIn patients with CAD, the relative proportion of the CD14(++)CD16(-) monocyte subset was elevated (P<0.05) and of the CD14(+)CD16(++) subset was reduced (P<0.001) compared with the HBD group. Furthermore, MPA formation significantly increased in patients with CAD in all three monocyte subsets. In both study groups, the majority of CCR5(+) cells was detected in CD14(++)CD16(+) monocytes (P<0.001 versus CD14(++)CD16(-) and CD14(+)CD16(++)), although the CCR5(+) monocyte number was reduced in patients with CAD (CD14(++)CD16(-)/CD14(+)CD16(++), P<0.001; CD14(++)CD16(+), P<0.05) compared with the HBD group, particularly in those who were not taking statins. Ex vivo incubation of monocytes from HBDs with plasma from patients with CAD also decreased CCR5(+) expression (P<0.05 versus plasma from HBDs). Serum CCL5 levels were similar in both groups. ConclusionsThe increased monocyte-platelet cross-talk in patients with CAD might have contributed to atherosclerosis progression. The decreased CCR5(+) monocyte numbers in patients with CAD could have resulted from CCR5(+) cell recruitment into atherosclerotic lesions or CCR5 downregulation in response to circulating factors."],["dc.identifier.doi","10.1111/joim.12145"],["dc.identifier.gro","3142194"],["dc.identifier.isi","000329764500006"],["dc.identifier.pmid","24118494"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/5577"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: University Medical Center Gottingen"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1365-2796"],["dc.relation.issn","0954-6820"],["dc.title","Increased proatherogenic monocyte-platelet cross-talk in monocyte subpopulations of patients with stable coronary artery disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2016Conference Abstract [["dc.bibliographiccitation.journal","Der Internist"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Czepluch, Frauke S."],["dc.contributor.author","Schwarz, A."],["dc.contributor.author","Tichelbaecker, Tobias"],["dc.contributor.author","Lotz, Joachim"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Schillinger, Wolfgang"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.date.accessioned","2018-11-07T10:15:50Z"],["dc.date.available","2018-11-07T10:15:50Z"],["dc.date.issued","2016"],["dc.format.extent","S40"],["dc.identifier.isi","000375417500075"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40896"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.issn","1432-1289"],["dc.relation.issn","0020-9554"],["dc.title","The transfemoral Implantation of a 29 mm metal-free Aortic Valve Bioprosthesis in the elderly is associated with longer Procedure times and post interventional higher Flaps-Gradient"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details WOS2018Journal Article [["dc.bibliographiccitation.firstpage","790"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Der Internist"],["dc.bibliographiccitation.lastpage","798"],["dc.bibliographiccitation.volume","59"],["dc.contributor.author","Czepluch, F."],["dc.contributor.author","Hasenfuß, G."],["dc.contributor.author","Wollnik, B."],["dc.date.accessioned","2020-12-10T14:08:24Z"],["dc.date.available","2020-12-10T14:08:24Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1007/s00108-018-0452-z"],["dc.identifier.eissn","1432-1289"],["dc.identifier.issn","0020-9554"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70451"],["dc.language.iso","de"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Moderne humangenetische Beratung"],["dc.title.alternative","Modern genetic counselling. Practical aspects exemplified by hypertrophic cardiomyopathy"],["dc.title.subtitle","Praktische Aspekte am Beispiel der hypertrophen Kardiomyopathie"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2016Journal Article [["dc.bibliographiccitation.firstpage","281"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","The Journal of heart valve disease"],["dc.bibliographiccitation.lastpage","288"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Czepluch, Frauke S."],["dc.contributor.author","Schwarz, Alexander"],["dc.contributor.author","Tichelbäcker, Tobias"],["dc.contributor.author","Lotz, Joachim"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Schillinger, Wolfgang"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.date.accessioned","2017-10-27T11:17:58Z"],["dc.date.available","2017-10-27T11:17:58Z"],["dc.date.issued","2016"],["dc.description.abstract","The Direct Flow Medical (DFM) valve is a new non-metallic and repositionable bioprosthesis used for transcatheter aortic valve implantation (TAVI). The study aim was to investigate procedural and post-implant valve data in patients receiving differently sized DFM bioprostheses."],["dc.identifier.fs","623793"],["dc.identifier.pmid","27989037"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/9886"],["dc.language.iso","en"],["dc.notes.status","fcwi"],["dc.title","Predictors of High Post-Procedural Gradients after Catheter-Based Aortic Valve Implantation Using Direct Flow Medical Bioprostheses"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]Details PMID PMC2013Journal Article Discussion [["dc.bibliographiccitation.firstpage","1080"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Thrombosis and Haemostasis"],["dc.bibliographiccitation.lastpage","1082"],["dc.bibliographiccitation.volume","110"],["dc.contributor.author","Czepluch, Frauke S."],["dc.contributor.author","Kuschicke, Hendrik"],["dc.contributor.author","Dellas, Claudia"],["dc.contributor.author","Riggert, Joachim"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Schaefer, Katrin"],["dc.date.accessioned","2017-09-07T11:47:04Z"],["dc.date.available","2017-09-07T11:47:04Z"],["dc.date.issued","2013"],["dc.identifier.doi","10.1160/TH13-05-0367"],["dc.identifier.gro","3142259"],["dc.identifier.isi","000326991900026"],["dc.identifier.pmid","23884216"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/6298"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Schattauer Gmbh-verlag Medizin Naturwissenschaften"],["dc.relation.issn","0340-6245"],["dc.title","Atheroprotective Kruppel-like factor 4 is downregulated in monocyte subsets of patients with coronary artery disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2014Journal Article Research Paper [["dc.bibliographiccitation.firstpage","148"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Microcirculation"],["dc.bibliographiccitation.lastpage","158"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Czepluch, Frauke S."],["dc.contributor.author","Bernhardt, Markus"],["dc.contributor.author","Kuschicke, Hendrik"],["dc.contributor.author","Gogiraju, Rajinikanth"],["dc.contributor.author","Schroeter, Marco R."],["dc.contributor.author","Riggert, Joachim"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Schaefer, Katrin"],["dc.date.accessioned","2017-09-07T11:46:33Z"],["dc.date.available","2017-09-07T11:46:33Z"],["dc.date.issued","2014"],["dc.description.abstract","ObjectiveHuman monocytes can be divided into CD16(-) monocytes and CD16(+) monocytes. Studies in mice suggested differential effects of monocyte subsets during new vessel formation. MethodsThe functional role of human monocyte subsets in neovascularization processes was investigated. For in vivo experiments, nude mice underwent unilateral hindlimb ischemia surgery before being injected with either total monocytes, CD16(-) monocytes or CD16(+) monocytes isolated from healthy individuals. ResultsIn vitro, cytokine array analysis demonstrated that monocytes release numerous angiogenic cytokines, some of which were differentially expressed in monocyte subsets. Sprout length was enhanced in EC spheroids being cultured in conditioned medium obtained from total monocytes and, to a lesser extent, also in supernatants of CD16(-) monocytes. Laser Doppler perfusion imaging up to day 28 after surgery revealed a trend toward improved revascularization in mice treated with monocytes, but no significant differences between monocyte subsets. Histological analyses four weeks after surgery showed an increased arteriole size in mice having received CD16(+) monocytes, whereas the number of capillaries did not significantly differ between groups. ConclusionsOur findings suggest additive and differential effects of monocyte subsets during neovascularization processes, possibly due to an altered secretion of angiogenic factors and their paracrine capacity to stimulate new vessel formation."],["dc.identifier.doi","10.1111/micc.12100"],["dc.identifier.gro","3142188"],["dc.identifier.isi","000331339000007"],["dc.identifier.pmid","24125396"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/5510"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: University Medical Center Gottingen"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1549-8719"],["dc.relation.issn","1073-9688"],["dc.title","In Vitro and In Vivo Effects of Human Monocytes and their Subsets on New Vessel Formation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2018Journal Article [["dc.bibliographiccitation.firstpage","1063"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Der Internist"],["dc.bibliographiccitation.lastpage","1073"],["dc.bibliographiccitation.volume","59"],["dc.contributor.author","Czepluch, Frauke S."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2020-12-10T14:08:24Z"],["dc.date.available","2020-12-10T14:08:24Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1007/s00108-018-0485-3"],["dc.identifier.eissn","1432-1289"],["dc.identifier.issn","0020-9554"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70453"],["dc.language.iso","de"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Genetische Herzerkrankungen und Speichererkrankungen mit kardialer Beteiligung"],["dc.title.alternative","Inherited heart diseases and storage diseases with cardiac involvement"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2018Journal Article [["dc.bibliographiccitation.firstpage","211"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","ESC Heart Failure"],["dc.bibliographiccitation.lastpage","217"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Czepluch, Frauke S."],["dc.contributor.author","Wollnik, Bernd"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2018-04-23T11:49:07Z"],["dc.date.available","2018-04-23T11:49:07Z"],["dc.date.issued","2018"],["dc.description.abstract","The relevance of gene mutations leading to heart diseases and hence heart failure has become evident. The risk for and the course of heart failure depends on genomic variants and mutations underlying the so‐called genetic predisposition. Genetic contribution to heart failure is highly heterogenous and complex. For any patient with a likely inherited heart failure syndrome, genetic counselling is recommended and important. In the last few years, novel sequencing technologies (named next‐generation sequencing – NGS) have dramatically improved the availability of molecular testing, the efficiency of genetic analyses, and moreover reduced the cost for genetic testing. Due to this development, genetic testing has become increasingly accessible and NGS‐based sequencing is now applied in clinical routine diagnostics. One of the most common reasons of heart failure are cardiomyopathies such as the dilated or the hypertrophic cardiomyopathy. Nearly 100 disease‐associated genes have been identified for cardiomyopathies. The knowledge of a pathogenic mutation can be used for genetic counselling, risk and prognosis determination, therapy guidance and hence for a more effective treatment. Besides, family cascade screening for a known familial, pathogenic mutation can lead to an early diagnosis in affected individuals. At that timepoint, a preventative intervention could be used to avoid or delay disease onset or delay disease progression. Understanding the cellular basis of genetic heart failure syndromes in more detail may provide new insights into the molecular biology of physiological and impaired cardiac (cell) function. As our understanding of the molecular and genetic pathophysiology of heart failure will increase, this might help to identify novel therapeutic targets and may lead to the development of new and specific treatment options in patients with heart failure."],["dc.identifier.doi","10.1002/ehf2.12267"],["dc.identifier.gro","3142497"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13650"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.status","final"],["dc.relation.issn","2055-5822"],["dc.title","Genetic determinants of heart failure: facts and numbers"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]Details DOI2012Conference Abstract [["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Czepluch, Frauke S."],["dc.contributor.author","Kuschicke, H."],["dc.contributor.author","Schlegel, Mathias"],["dc.contributor.author","Mueller, M."],["dc.contributor.author","Bernhardt, M."],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Riggert, Joachim"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Schaefer, K."],["dc.date.accessioned","2018-11-07T09:07:30Z"],["dc.date.available","2018-11-07T09:07:30Z"],["dc.date.issued","2012"],["dc.format.extent","750"],["dc.identifier.isi","000308012405357"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25808"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.publisher.place","Oxford"],["dc.relation.eventlocation","Munchen, GERMANY"],["dc.relation.issn","0195-668X"],["dc.title","Krueppel-like factor 4 is downregulated in circulating monocyte subsets of patients with Coronary Artery Disease"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details WOS