Zeisberg, Elisabeth M.

[["dc.bibliographiccitation.firstpage","S18"],["dc.bibliographiccitation.journal","Der Internist"],["dc.bibliographiccitation.lastpage","S19"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Alnour, Fouzi"],["dc.contributor.author","Xu, X."],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.date.accessioned","2018-11-07T10:15:49Z"],["dc.date.available","2018-11-07T10:15:49Z"],["dc.date.issued","2016"],["dc.identifier.isi","000375417500031"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40892"],["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","KIAA0182: a new gene relevant for cardiac development"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","225"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Differentiation"],["dc.bibliographiccitation.lastpage","236"],["dc.bibliographiccitation.volume","92"],["dc.contributor.author","Liu, Xiaopeng"],["dc.contributor.author","Qi, Jing"],["dc.contributor.author","Xu, X."],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Guan-Schmidt, Kaomei"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.date.accessioned","2018-11-07T10:07:27Z"],["dc.date.available","2018-11-07T10:07:27Z"],["dc.date.issued","2016"],["dc.description.abstract","Endothelial cells derived from human induced pluripotent stem cells (hiPSC-EC) are of significant value for research on human vascular development, in vitro disease models and drug screening. Here we report an alternative, highly efficient and cost-effective simple three step method (mesoderm induction, endothelial cell differentiation and endothelial cell expansion) to differentiate hiPSC directly into endothelial cells. We demonstrate that efficiency of described method to derive CD31 + and VE-Cadherin+ double positive cells is higher than 80% in 12 days. Most notably we established that hiPSC-EC differentiation efficacy depends on optimization of both mesoderm differentiation and endothelial cell differentiation steps. (C) 2016 International Society of Differentiation. Published by Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.diff.2016.05.004"],["dc.identifier.isi","000387936500010"],["dc.identifier.pmid","27266810"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39283"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/329"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1432-0436"],["dc.relation.issn","0301-4681"],["dc.title","Differentiation of functional endothelial cells from human induced pluripotent stem cells: A novel, highly efficient and cost effective method"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","459"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Biochemical and Biophysical Research Communications"],["dc.bibliographiccitation.lastpage","464"],["dc.bibliographiccitation.volume","472"],["dc.contributor.author","Tan, Xiaoying"],["dc.contributor.author","Xu, X."],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Zeisberg, Michael"],["dc.date.accessioned","2018-11-07T10:15:34Z"],["dc.date.available","2018-11-07T10:15:34Z"],["dc.date.issued","2016"],["dc.description.abstract","Phosphate is an essential constituent of critical cellular functions including energy metabolism, nucleic acid synthesis and phosphorylation-dependent cell signaling. Increased plasma phosphate levels are an independent risk factor for lowered life-expectancy as well as for heart and kidney failure. Nevertheless, direct cellular effects of elevated phosphate concentrations within the microenvironment are poorly understood and have been largely neglected in favor of phosphor-regulatory hormones. Because interstitial fibrosis is the common determinant of chronic progressive kidney disease, and because fibroblasts are major mediators of fibrogenesis, we here explored the effect of high extracellular phosphate levels on renal fibroblasts. We demonstrate that high inorganic phosphate directly induces fibrotic fibroblast activation associated with increased proliferative activity, increased expression of alpha-smooth muscle actin and increased synthesis of type I collagen. We further demonstrate that such fibroblast activation is dependent on phosphate influx, aberrant phosphorylation of DNA methyltransferase DNMT1 and aberrant CpG island promoter methylation. In summary, our studies demonstrate that elevated phosphate concentrations induce pro-fibrotic fibroblast activation independent of phospho-regulatory hormones. (C) 2016 Published by Elsevier Inc."],["dc.identifier.doi","10.1016/j.bbrc.2016.01.077"],["dc.identifier.isi","000373523300009"],["dc.identifier.pmid","26774342"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40839"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/138"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C01: Epigenetische Kontrolle der Herzfibrose"],["dc.relation.issn","1090-2104"],["dc.relation.issn","0006-291X"],["dc.relation.workinggroup","RG E. Zeisberg (Kardiales Stroma)"],["dc.relation.workinggroup","RG M. Zeisberg (Renale Fibrogenese)"],["dc.title","High inorganic phosphate causes DNMT1 phosphorylation and subsequent fibrotic fibroblast activation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1222"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","FEBS Letters"],["dc.bibliographiccitation.lastpage","1233"],["dc.bibliographiccitation.volume","590"],["dc.contributor.author","Xu, X."],["dc.contributor.author","Tan, Xiaoying"],["dc.contributor.author","Hulshoff, Melanie S."],["dc.contributor.author","Wilhelmi, Tim"],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.date.accessioned","2018-11-07T10:16:06Z"],["dc.date.available","2018-11-07T10:16:06Z"],["dc.date.issued","2016"],["dc.description.abstract","Cardiac fibrosis is integral in chronic heart disease, and one of the cellular processes contributing to cardiac fibrosis is endothelial-to-mesenchymal transition (EndMT). We recently found that hypoxia efficiently induces human coronary artery endothelial cells (HCAEC) to undergo EndMT through a hypoxia inducible factor-1 alpha (HIF1 alpha)-dependent pathway. Promoter hypermethylation of Ras-Gap-like protein 1 (RASAL1) has also been recently associated with EndMT progression and cardiac fibrosis. Our findings suggest that HIF1 alpha and transforming growth factor (TGF)/SMAD signalling pathways synergistically regulate hypoxia-induced EndMT through both DNMT3a-mediated hypermethylation of RASAL1 promoter and direct SNAIL induction. The findings indicate that multiple cascades may be activated simultaneously to mediate hypoxia-induced EndMT."],["dc.identifier.doi","10.1002/1873-3468.12158"],["dc.identifier.isi","000375008700019"],["dc.identifier.pmid","27012941"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40968"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley"],["dc.relation.issn","1873-3468"],["dc.title","Hypoxia-induced endothelial-mesenchymal transition is associated with RASAL1 promoter hypermethylation in human coronary endothelial cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Der Internist"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Tan, X."],["dc.contributor.author","Xu, X."],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Zeisberg, Michael"],["dc.date.accessioned","2018-11-07T10:15:56Z"],["dc.date.available","2018-11-07T10:15:56Z"],["dc.date.issued","2016"],["dc.format.extent","S3"],["dc.identifier.isi","000375417500002"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40925"],["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","High Phosphate Induces Endothelial-Mesenchymal Transition of Human Coronary Endothelial Cells by Epigenetic Regulation of DNMT1: a Link from Chronic Kidney to Cardiovascular Disease"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S20"],["dc.bibliographiccitation.journal","Der Internist"],["dc.bibliographiccitation.lastpage","S21"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Xu, X."],["dc.contributor.author","Tan, X."],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Zeisberg, Elisabeth"],["dc.date.accessioned","2018-11-07T10:15:57Z"],["dc.date.available","2018-11-07T10:15:57Z"],["dc.date.issued","2016"],["dc.identifier.isi","000375417500036"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40930"],["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","Hypoxia induced endothelial to mesenchymal transition is associated with promoter hypermethylation in human RASAL1 coronary endothelial cells."],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","905"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Journal of the American Society of Nephrology"],["dc.bibliographiccitation.lastpage","912"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Tampe, Björn"],["dc.contributor.author","Tampe, Desiree"],["dc.contributor.author","Müller, Claudia A."],["dc.contributor.author","Sugimoto, Hikaru"],["dc.contributor.author","LeBleu, Valerie S."],["dc.contributor.author","Xu, X."],["dc.contributor.author","Müller, Georg Anton"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Kalluri, Raghu"],["dc.contributor.author","Zeisberg, Michael"],["dc.date.accessioned","2018-11-07T09:40:40Z"],["dc.date.available","2018-11-07T09:40:40Z"],["dc.date.issued","2014"],["dc.description.abstract","Research funding from public and private sources has reached an all-time low. Economic conditions, sequestration, and a trend of low award success rates have created an imbalance between the supply of highly qualified research investigators and the availability of critically necessary research dollars. This grim environment continues to hinder the success of established investigators and deter potential investigators from joining the research workforce. Without action and support of innovative science, the future of the US health care system is in jeopardy, and its leadership role in medical research will decrease. This work discusses the effects of the decline in research funding, the plight of kidney research, and the impact of the American Society of Nephrology Grants Program on scientists. The ASN also calls on the entire nephrology community to rejuvenate the research environment, improve the lives of millions of people with kidney disease, and ultimately, find a cure."],["dc.identifier.doi","10.1681/ASN.2013070723"],["dc.identifier.isi","000335583700010"],["dc.identifier.pmid","24480825"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33556"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/113"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C01: Epigenetische Kontrolle der Herzfibrose"],["dc.relation.issn","1533-3450"],["dc.relation.issn","1046-6673"],["dc.relation.workinggroup","RG E. Zeisberg (Kardiales Stroma)"],["dc.relation.workinggroup","RG M. Zeisberg (Renale Fibrogenese)"],["dc.title","Tet3-Mediated Hydroxymethylation of Epigenetically Silenced Genes Contributes to Bone Morphogenic Protein 7-Induced Reversal of Kidney Fibrosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","16653"],["dc.bibliographiccitation.issue","27"],["dc.bibliographiccitation.journal","Journal of Biological Chemistry"],["dc.bibliographiccitation.lastpage","16664"],["dc.bibliographiccitation.volume","290"],["dc.contributor.author","Xu, X."],["dc.contributor.author","Tan, Xiaoying"],["dc.contributor.author","Tampe, Björn"],["dc.contributor.author","Sanchez, Elisa"],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.date.accessioned","2018-11-07T09:54:45Z"],["dc.date.available","2018-11-07T09:54:45Z"],["dc.date.issued","2015"],["dc.description.abstract","Endothelial to mesenchymal transition (EndMT) was originally described in heart development where the endocardial endothelial cells that line the atrioventricular canal undergo an EndMT to form the endocardial mesenchymal cushion that later gives rise to the septum and mitral and tricuspid valves. In the postnatal heart specifically, endothelial cells that originate from the endocardium maintain increased susceptibility to undergo EndMT as remnants from their embryonic origin. Such EndMT involving adult coronary endothelial cells contributes to microvascular rarefaction and subsequent chronification of hypoxia in the injured heart, ultimately leading to cardiac fibrosis. Although in most endothelial beds hypoxia induces tip cell formation and sprouting angiogenesis, here we demonstrate that hypoxia is a stimulus for human coronary endothelial cells to undergo phenotypic changes reminiscent of EndMT via a mechanism involving hypoxia-inducible factor 1 alpha-induced activation of the EndMT master regulatory transcription factor SNAIL. Our study adds further evidence for the unique susceptibility of endocardium-derived endothelial cells to undergo EndMT and provides novel insights into how hypoxia contributes to progression of cardiac fibrosis. Additional studies may be required to discriminate between distinct sprouting angiogenesis and EndMT responses of different endothelial cells populations."],["dc.identifier.doi","10.1074/jbc.M115.636944"],["dc.identifier.isi","000357572800016"],["dc.identifier.pmid","25971970"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36606"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Biochemistry Molecular Biology Inc"],["dc.relation.issn","1083-351X"],["dc.relation.issn","0021-9258"],["dc.title","Snail Is a Direct Target of Hypoxia-inducible Factor 1 alpha (HIF1 alpha) in Hypoxia-induced Endothelial to Mesenchymal Transition of Human Coronary Endothelial Cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","99"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","International Journal of Cardiology"],["dc.bibliographiccitation.lastpage","109"],["dc.bibliographiccitation.volume","176"],["dc.contributor.author","Charytan, David M."],["dc.contributor.author","Padera, Robert F."],["dc.contributor.author","Helfand, Alexander M."],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Xu, X."],["dc.contributor.author","Liu, Xiaopeng"],["dc.contributor.author","Himmelfarb, Jonathan"],["dc.contributor.author","Cinelli, Angeles"],["dc.contributor.author","Kalluri, Raghu"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.date.accessioned","2018-11-07T09:36:08Z"],["dc.date.available","2018-11-07T09:36:08Z"],["dc.date.issued","2014"],["dc.description.abstract","Background: Sudden cardiovascular death is increased in chronic kidney disease (CKD). Experimental CKD models suggest that angiogenesis and nitric oxide (NO) inhibitors induce myocardial fibrosis and microvascular dropout thereby facilitating arrhythmogenesis. We undertook this study to characterize associations of CKD with human myocardial pathology, NO-related circulating angiogenesis inhibitors, and endothelial cell behavior. Methods: We compared heart (n = 54) and serum (n = 162) samples from individuals with and without CKD, and assessed effects of serum on human coronary artery endothelial cells (HCAECs) in vitro. Left ventricular fibrosis and capillary density were quantified in post-mortem samples. Endothelial to mesenchymal transition (EndMT) was assessed by immunostaining of post-mortem samples and RNA expression in heart tissue obtained during cardiac surgery. Circulating asymmetric dimethylarginine (ADMA), endostatin (END), angiopoietin-2 (ANG), and thrombospondin-2 (TSP) were measured, and the effect of these factors and of subject serum on proliferation, apoptosis, and EndMT of HCAEC was analyzed. Results: Cardiac fibrosis increased 12% and 77% in stage 3-4 CKD and ESRD and microvascular density decreased 12% and 16% vs. preserved renal function. EndMT-derived fibroblast proportion was 17% higher in stage 3-4 CKD and ESRD (P-trend = 0.02). ADMA, ANG, TSP, and END concentrations increased in CKD. Both individual factors and CKD serum increased HCAEC apoptosis (P = 0.02), decreased proliferation (P = 0.03), and induced EndMT. Conclusions: CKD is associated with an increase in circulating angiogenesis and NO inhibitors, which impact proliferation and apoptosis of cardiac endothelial cells and promote EndMT, leading to cardiac fibrosis and capillary rarefaction. These processes may play key roles in CKD-associated CV disease. (C) 2014 Elsevier Ireland Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.ijcard.2014.06.062"],["dc.identifier.isi","000341040900026"],["dc.identifier.pmid","25049013"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32544"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/6"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C01: Epigenetische Kontrolle der Herzfibrose"],["dc.relation.issn","1874-1754"],["dc.relation.issn","0167-5273"],["dc.relation.workinggroup","RG E. Zeisberg (Kardiales Stroma)"],["dc.relation.workinggroup","RG M. Zeisberg (Renale Fibrogenese)"],["dc.title","Increased concentration of circulating angiogenesis and nitric oxide inhibitors induces endothelial to mesenchymal transition and myocardial fibrosis in patients with chronic kidney disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]