Cyganek, Lukas

[["dc.bibliographiccitation.firstpage","975"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Journal of the American College of Cardiology"],["dc.bibliographiccitation.lastpage","991"],["dc.bibliographiccitation.volume","70"],["dc.contributor.author","Borchert, Thomas"],["dc.contributor.author","Hübscher, Daniela"],["dc.contributor.author","Guessoum, Celina I."],["dc.contributor.author","Lam, Tuan-Dinh D."],["dc.contributor.author","Ghadri, Jelena R."],["dc.contributor.author","Schellinger, Isabel N."],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Liaw, Norman Y."],["dc.contributor.author","Li, Yun"],["dc.contributor.author","Haas, Jan"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Huber, Mia A."],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Raaz, Uwe"],["dc.contributor.author","Nikolaev, Viacheslav O."],["dc.contributor.author","Guan, Kaomei"],["dc.contributor.author","Thiele, Holger"],["dc.contributor.author","Meder, Benjamin"],["dc.contributor.author","Wollnik, Bernd"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Lüscher, Thomas F."],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Templin, Christian"],["dc.contributor.author","Streckfuss-Bömeke, Katrin"],["dc.date.accessioned","2018-04-23T11:48:11Z"],["dc.date.available","2018-04-23T11:48:11Z"],["dc.date.issued","2017"],["dc.description.abstract","Background Takotsubo syndrome (TTS) is characterized by an acute left ventricular dysfunction and is associated with life-threating complications in the acute phase. The underlying disease mechanism in TTS is still unknown. A genetic basis has been suggested to be involved in the pathogenesis. Objectives The aims of the study were to establish an in vitro induced pluripotent stem cell (iPSC) model of TTS, to test the hypothesis of altered β-adrenergic signaling in TTS iPSC-cardiomyocytes (CMs), and to explore whether genetic susceptibility underlies the pathophysiology of TTS. Methods Somatic cells of patients with TTS and control subjects were reprogrammed to iPSCs and differentiated into CMs. Three-month-old CMs were subjected to catecholamine stimulation to simulate neurohumoral overstimulation. We investigated β-adrenergic signaling and TTS cardiomyocyte function. Results Enhanced β-adrenergic signaling in TTS-iPSC-CMs under catecholamine-induced stress increased expression of the cardiac stress marker NR4A1; cyclic adenosine monophosphate levels; and cyclic adenosine monophosphate–dependent protein kinase A–mediated hyperphosphorylation of RYR2-S2808, PLN-S16, TNI-S23/24, and Cav1.2-S1928, and leads to a reduced calcium time to transient 50% decay. These cellular catecholamine-dependent responses were mainly mediated by β1-adrenoceptor signaling in TTS. Engineered heart muscles from TTS-iPSC-CMs showed an impaired force of contraction and a higher sensitivity to isoprenaline-stimulated inotropy compared with control subjects. In addition, altered electrical activity and increased lipid accumulation were detected in catecholamine-treated TTS-iPSC-CMs, and were confirmed by differentially expressed lipid transporters CD36 and CPT1C. Furthermore, we uncovered genetic variants in different key regulators of cardiac function. Conclusions Enhanced β-adrenergic signaling and higher sensitivity to catecholamine-induced toxicity were identified as mechanisms associated with the TTS phenotype."],["dc.identifier.doi","10.1016/j.jacc.2017.06.061"],["dc.identifier.gro","3142333"],["dc.identifier.pmid","28818208"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16489"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13468"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/204"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | D01: Erholung aus der Herzinsuffizienz – Einfluss von Fibrose und Transkriptionssignatur"],["dc.relation","SFB 1002 | D02: Neue Mechanismen der genomischen Instabilität bei Herzinsuffizienz"],["dc.relation.issn","0735-1097"],["dc.relation.workinggroup","RG Cyganek (Stem Cell Unit)"],["dc.relation.workinggroup","RG Dressel"],["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 Nikolaev (Cardiovascular Research Center)"],["dc.relation.workinggroup","RG Sossalla (Kardiovaskuläre experimentelle Elektrophysiologie und Bildgebung)"],["dc.relation.workinggroup","RG Tiburcy (Stem Cell Disease Modeling)"],["dc.relation.workinggroup","RG Wollnik"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Catecholamine-Dependent β-Adrenergic Signaling in a Pluripotent Stem Cell Model of Takotsubo Cardiomyopathy"],["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"]]

[["dc.bibliographiccitation.artnumber","101560"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","STAR Protocols"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Lyra-Leite, Davi M."],["dc.contributor.author","Gutiérrez-Gutiérrez, Óscar"],["dc.contributor.author","Wang, Meimei"],["dc.contributor.author","Zhou, Yang"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Burridge, Paul W."],["dc.date.accessioned","2022-08-24T05:30:58Z"],["dc.date.available","2022-08-24T05:30:58Z"],["dc.date.issued","2022"],["dc.description.abstract","The methods for the culture and cardiomyocyte differentiation of human embryonic stem cells, and later human induced pluripotent stem cells (hiPSC), have moved from a complex and uncontrolled systems to simplified and relatively robust protocols, using the knowledge and cues gathered at each step. HiPSC-derived cardiomyocytes have proven to be a useful tool in human disease modelling, drug discovery, developmental biology, and regenerative medicine. In this protocol review, we will highlight the evolution of protocols associated with hPSC culture, cardiomyocyte differentiation, sub-type specification, and cardiomyocyte maturation. We also discuss protocols for somatic cell direct reprogramming to cardiomyocyte-like cells."],["dc.identifier.doi","10.1016/j.xpro.2022.101560"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/113149"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/543"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/443"],["dc.language.iso","en"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation.issn","2666-1667"],["dc.relation.workinggroup","RG Cyganek (Stem Cell Unit)"],["dc.rights","CC BY-NC-ND 4.0"],["dc.title","A review of protocols for human iPSC culture, cardiac differentiation, subtype-specification, maturation, and direct reprogramming"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Open Journal of Bioresources"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Beuthner, Bo E. C."],["dc.contributor.author","Topci, Rodi"],["dc.contributor.author","Derks, Mareike"],["dc.contributor.author","Franke, Thomas"],["dc.contributor.author","Seelke, Sandra"],["dc.contributor.author","Puls, Miriam"],["dc.contributor.author","Schuster, Andreas"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Valentova, Miroslava"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Nußbeck, Sara Y."],["dc.date.accessioned","2020-06-16T13:21:23Z"],["dc.date.available","2020-06-16T13:21:23Z"],["dc.date.issued","2020"],["dc.description.abstract","The bioresource (>265 patients with >27,600 biospecimens until December 2019; recruitment ongoing) on severe aortic stenosis is of vital importance to improve the still incomplete understanding of its etiology as well as its transition to heart failure. The bioresource contains various biospecimens, standardised clinical and imaging data sets including transthoracic echocardiography, computed tomography and magnetic resonance imaging of the heart. Biospecimen sampling follows the SOP-driven collection scheme of the German Center for Cardiovascular Research (DZHK) for venous blood and urine [1]. In addition, left-ventricular endomyocardial biopsies, rectal swabs and skin biopsies (for subsequent generation of induced pluripotent stem cells) are collected. Data management includes the use of a professional biospecimen management system as well as a Picture Archiving and Communication System (PACS) for imaging data. A Good Clinical Practice (GCP)-conform software for the management of clinical data and a trusted third party for the management of patient identifying data and pseudonyms are in place. Given these conditions, there is a high reuse-potential for biospecimens and data."],["dc.identifier.doi","10.5334/ojb.65"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/66366"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/340"],["dc.language.iso","en"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | D01: Erholung aus der Herzinsuffizienz – Einfluss von Fibrose und Transkriptionssignatur"],["dc.relation","SFB 1002 | INF: Unterstützung der SFB 1002 Forschungsdatenintegration, -visualisierung und -nachnutzung"],["dc.relation.issn","2056-5542"],["dc.relation.workinggroup","RG Cyganek (Stem Cell Unit)"],["dc.relation.workinggroup","RG E. Zeisberg (Kardiales Stroma)"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Nußbeck"],["dc.relation.workinggroup","RG Toischer (Kardiales Remodeling)"],["dc.rights","CC BY 3.0"],["dc.title","Interdisciplinary Research on Aortic Valve Stenosis: A Longitudinal Collection of Biospecimens and Clinical Data of Patients Undergoing Transcatheter Aortic Valve Replacement"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1621"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Journal of Bone and Mineral Research"],["dc.bibliographiccitation.lastpage","1635"],["dc.bibliographiccitation.volume","36"],["dc.contributor.affiliation","Rössler, Uta; 1\r\nBIH Center for Regenerative Therapies (BCRT)\r\nCharité ‐ Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt‐Universität zu Berlin, and Berlin Institute of Health\r\nBerlin Germany"],["dc.contributor.affiliation","Stelzer, Nina; 1\r\nBIH Center for Regenerative Therapies (BCRT)\r\nCharité ‐ Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt‐Universität zu Berlin, and Berlin Institute of Health\r\nBerlin Germany"],["dc.contributor.affiliation","Bose, Shroddha; 6\r\nInstitute of Chemistry and Biochemistry\r\nFreie Universität Berlin\r\nBerlin Germany"],["dc.contributor.affiliation","Kopp, Johannes; 1\r\nBIH Center for Regenerative Therapies (BCRT)\r\nCharité ‐ Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt‐Universität zu Berlin, and Berlin Institute of Health\r\nBerlin Germany"],["dc.contributor.affiliation","Søe, Kent; 8\r\nClinical Cell Biology, Department of Pathology\r\nOdense University Hospital\r\nOdense C Denmark"],["dc.contributor.affiliation","Cyganek, Lukas; 11\r\nStem Cell Unit, Clinic for Cardiology and Pneumology\r\nUniversity Medical Center Göttingen\r\nGöttingen Germany"],["dc.contributor.affiliation","Zifarelli, Giovanni; 13\r\nIstituto di Biofisica, CNR\r\nGenoa Italy"],["dc.contributor.affiliation","Ali, Salaheddine; 1\r\nBIH Center for Regenerative Therapies (BCRT)\r\nCharité ‐ Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt‐Universität zu Berlin, and Berlin Institute of Health\r\nBerlin Germany"],["dc.contributor.affiliation","von der Hagen, Maja; 14\r\nAbteilung Neuropädiatrie, Medizinische Fakultät Carl Gustav Carus\r\nTechnische Universität Dresden\r\nDresden Germany"],["dc.contributor.affiliation","Strässler, Elisabeth Tamara; 15\r\nDepartment of Cardiology\r\nCharité ‐ Universitätsmedizin Berlin, Campus Benjamin Franklin\r\nBerlin Germany"],["dc.contributor.affiliation","Hahn, Gabriele; 17\r\nInstitut und Poliklinik für Radiologische Diagnostik\r\nMedizinische Fakultät Carl Gustav Carus Technische Universität Dresden\r\nDresden Germany"],["dc.contributor.affiliation","Pusch, Michael; 13\r\nIstituto di Biofisica, CNR\r\nGenoa Italy"],["dc.contributor.affiliation","Stauber, Tobias; 6\r\nInstitute of Chemistry and Biochemistry\r\nFreie Universität Berlin\r\nBerlin Germany"],["dc.contributor.affiliation","Izsvák, Zsuzsanna; 19\r\nMax‐Delbrück‐Center for Molecular Medicine (MDC), Helmholtz Association\r\nBerlin Germany"],["dc.contributor.affiliation","Gossen, Manfred; 20\r\nBerlin‐Brandenburg Center for Regenerative Therapies\r\nCharité Virchow Campus\r\nBerlin Germany"],["dc.contributor.affiliation","Stachelscheid, Harald; 22\r\nCharité ‐ Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt‐Universität zu Berlin, and Berlin Institute of Health\r\nBerlin Germany"],["dc.contributor.author","Rössler, Uta"],["dc.contributor.author","Hennig, Anna Floriane"],["dc.contributor.author","Stelzer, Nina"],["dc.contributor.author","Bose, Shroddha"],["dc.contributor.author","Kopp, Johannes"],["dc.contributor.author","Søe, Kent"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Zifarelli, Giovanni"],["dc.contributor.author","Ali, Salaheddine"],["dc.contributor.author","Kornak, Uwe"],["dc.contributor.author","Pusch, Michael"],["dc.contributor.author","von der Hagen, Maja"],["dc.contributor.author","Strässler, Elisabeth Tamara"],["dc.contributor.author","Hahn, Gabriele"],["dc.contributor.author","Stauber, Tobias"],["dc.contributor.author","Izsvák, Zsuzsanna"],["dc.contributor.author","Gossen, Manfred"],["dc.contributor.author","Stachelscheid, Harald"],["dc.date.accessioned","2021-06-01T09:41:55Z"],["dc.date.available","2021-06-01T09:41:55Z"],["dc.date.issued","2021"],["dc.date.updated","2022-02-09T13:20:40Z"],["dc.description.abstract","ABSTRACT Human induced pluripotent stem cells (hiPSCs) hold great potential for modeling human diseases and the development of innovative therapeutic approaches. Here, we report on a novel, simplified differentiation method for forming functional osteoclasts from hiPSCs. The three‐step protocol starts with embryoid body formation, followed by hematopoietic specification, and finally osteoclast differentiation. We observed continuous production of monocyte‐like cells over a period of up to 9 weeks, generating sufficient material for several osteoclast differentiations. The analysis of stage‐specific gene and surface marker expression proved mesodermal priming, the presence of monocyte‐like cells, and of terminally differentiated multinucleated osteoclasts, able to form resorption pits and trenches on bone and dentine in vitro. In comparison to peripheral blood mononuclear cell (PBMC)‐derived osteoclasts hiPSC‐derived osteoclasts were larger and contained a higher number of nuclei. Detailed functional studies on the resorption behavior of hiPSC‐osteoclasts indicated a trend towards forming more trenches than pits and an increase in pseudoresorption. We used hiPSCs from an autosomal recessive osteopetrosis (ARO) patient (BIHi002‐A, ARO hiPSCs) with compound heterozygous missense mutations p.(G292E) and p.(R403Q) in CLCN7, coding for the Cl−/H+‐exchanger ClC‐7, for functional investigations. The patient's leading clinical feature was a brain malformation due to defective neuronal migration. Mutant ClC‐7 displayed residual expression and retained lysosomal co‐localization with OSTM1, the gene coding for the osteopetrosis‐associated transmembrane protein 1, but only ClC‐7 harboring the mutation p.(R403Q) gave strongly reduced ion currents. An increased autophagic flux in spite of unchanged lysosomal pH was evident in undifferentiated ARO hiPSCs. ARO hiPSC‐derived osteoclasts showed an increased size compared to hiPSCs of healthy donors. They were not able to resorb bone, underlining a loss‐of‐function effect of the mutations. In summary, we developed a highly reproducible, straightforward hiPSC‐osteoclast differentiation protocol. We demonstrated that osteoclasts differentiated from ARO hiPSCs can be used as a disease model for ARO and potentially also other osteoclast‐related diseases. © 2021 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR)."],["dc.description.sponsorship","Berlin Institute of Health"],["dc.description.sponsorship","BCRT crossfield project GenoPro"],["dc.description.sponsorship","BIH Center for Regenerative Therapies"],["dc.description.sponsorship","European Community's Seventh Framework Programme"],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft http://dx.doi.org/10.13039/501100001659"],["dc.identifier.doi","10.1002/jbmr.4322"],["dc.identifier.pmid","33905594"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85075"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/394"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation.eissn","1523-4681"],["dc.relation.issn","0884-0431"],["dc.relation.workinggroup","RG Cyganek (Stem Cell Unit)"],["dc.rights","This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made."],["dc.title","Efficient generation of osteoclasts from human induced pluripotent stem cells and functional investigations of lethal CLCN7 ‐related osteopetrosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","008"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Journal of Clinical & Experimental Cardiology"],["dc.bibliographiccitation.lastpage","12"],["dc.bibliographiccitation.volume","S11"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Chen, Simin"],["dc.contributor.author","Borchert, Thomas"],["dc.contributor.author","Guan, Kaomei"],["dc.date.accessioned","2019-02-27T14:01:08Z"],["dc.date.available","2019-02-27T14:01:08Z"],["dc.date.issued","2013"],["dc.description.abstract","Heart disease is the principal cause of death in humans. Stem cell-based therapy for heart regeneration has long been seen as a potential application since the heart lacks adequate intrinsic regenerative potential. In the cardiovascular field, clinical trials have already been carried out by implantation of both bone marrow-derived stem cells and cardiac resident progenitor cells derived from the adult heart tissue into the injured myocardium to restore the functionality of the heart after damage. However, before a robust stem and progenitor cell-based therapy for cardiovascular diseases can be applied in the clinical setting, more research is necessary to generate sufficient quantities of functional cardiomyocytes from stem cells and to understand behavior of cardiomyocytes upon transplantation. A comprehensive understanding of the developmental processes involved in cardiogenesis might support further investigations in more efficient cell-based regeneration therapies. This review discusses the molecular aspects of cardiogenesis during early development and links the insights with the in vitro generation of cardiac progenitor cells as well as functional cardiomyocytes. Furthermore, we discuss the advantages of cardiac progenitor cells and cardiomyocytes derived from pluripotent stem cells, cardiac resident stem cells in regenerative applications to cope with the damaged heart."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2013"],["dc.identifier.doi","10.4172/2155-9880.S11-008"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9212"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57647"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/7"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["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.issn","2155-9880"],["dc.relation.workinggroup","RG Cyganek (Stem Cell Unit)"],["dc.relation.workinggroup","RG Guan (Application of patient-specific induced pluripotent stem cells in disease modelling)"],["dc.rights","CC BY-NC-ND 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/3.0"],["dc.title","Cardiac Progenitor Cells and their Therapeutic Application for Cardiac Repair"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","overview_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Cell and Developmental Biology"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Luo, Xiaojing"],["dc.contributor.author","Li, Wener"],["dc.contributor.author","Künzel, Karolina"],["dc.contributor.author","Henze, Sarah"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Strano, Anna"],["dc.contributor.author","Poetsch, Mareike S."],["dc.contributor.author","Schubert, Mario"],["dc.contributor.author","Guan, Kaomei"],["dc.date.accessioned","2021-04-14T08:23:52Z"],["dc.date.available","2021-04-14T08:23:52Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.3389/fcell.2020.00772"],["dc.identifier.pmid","32903370"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81078"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/367"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["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.eissn","2296-634X"],["dc.relation.workinggroup","RG Cyganek (Stem Cell Unit)"],["dc.relation.workinggroup","RG Guan (Application of patient-specific induced pluripotent stem cells in disease modelling)"],["dc.rights","CC BY 4.0"],["dc.title","IP3R-Mediated Compensatory Mechanism for Calcium Handling in Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes With Cardiac Ryanodine Receptor Deficiency"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","2935"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Yücel, Gökhan"],["dc.contributor.author","Zhao, Zhihan"],["dc.contributor.author","El-Battrawy, Ibrahim"],["dc.contributor.author","Lan, Huan"],["dc.contributor.author","Lang, Siegfried"],["dc.contributor.author","Li, Xin"],["dc.contributor.author","Buljubasic, Fanis"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Utikal, Jochen"],["dc.contributor.author","Ravens, Ursula"],["dc.contributor.author","Wieland, Thomas"],["dc.contributor.author","Borggrefe, Martin"],["dc.contributor.author","Zhou, Xiao-Bo"],["dc.contributor.author","Akin, Ibrahim"],["dc.date.accessioned","2018-04-23T11:49:22Z"],["dc.date.available","2018-04-23T11:49:22Z"],["dc.date.issued","2017"],["dc.description.abstract","Severe infections like sepsis lead frequently to cardiomyopathy. The mechanisms are unclear and an optimal therapy for septic cardiomyopathy still lacks. The aim of this study is to establish an endotoxin-induced inflammatory model using human induced pluripotent stem cell (hiPSC) derived cardiomyocytes (hiPSC-CMs) for mechanistic and therapeutic studies. hiPSC-CMs were treated by lipopolysaccharide (LPS) in different concentrations for different times. ELISA, FACS, qPCR, and patch-clamp techniques were used for the study. TLR4 (Toll-like receptor 4) and its associated proteins, CD14, LBP (lipopolysaccharide binding protein), TIRAP (toll-interleukin 1 receptor domain containing adaptor protein), Ly96 (lymphocyte antigen 96) and nuclear factor kappa B as well as some pro-and anti-inflammatory factors are expressed in hiPSC-CMs. LPS-treatment for 6 hours increased the expression levels of pro-inflammatory and chemotactic cytokines (TNF-a, IL-1ß, IL-6, CCL2, CCL5, IL-8), whereas 48 hour-treatment elevated the expression of anti-inflammatory factors (IL-10 and IL-6). LPS led to cell injury resulting from exaggerated cell apoptosis and necrosis. Finally, LPS inhibited small conductance Ca2+-activated K+ channel currents, enhanced Na+/Ca2+-exchanger currents, prolonged action potential duration, suggesting cellular electrical dysfunctions. Our data demonstrate that hiPSC-CMs possess the functional reaction system involved in endotoxin-induced inflammation and can model some bacterium-induced inflammatory responses in cardiac myocytes."],["dc.identifier.doi","10.1038/s41598-017-03147-4"],["dc.identifier.gro","3142526"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14783"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13682"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.issn","2045-2322"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Lipopolysaccharides induced inflammatory responses and electrophysiological dysfunctions in human-induced pluripotent stem cell derived cardiomyocytes"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","EMBO reports"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Yousefi, Roya"],["dc.contributor.author","Fornasiero, Eugenio F"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Montoya, Julio"],["dc.contributor.author","Jakobs, Stefan"],["dc.contributor.author","Rizzoli, Silvio O"],["dc.contributor.author","Rehling, Peter"],["dc.contributor.author","Pacheu‐Grau, David"],["dc.date.accessioned","2021-04-14T08:28:03Z"],["dc.date.available","2021-04-14T08:28:03Z"],["dc.date.issued","2021"],["dc.description.abstract","Abstract Mitochondria possess a small genome that codes for core subunits of the oxidative phosphorylation system and whose expression is essential for energy production. Information on the regulation and spatial organization of mitochondrial gene expression in the cellular context has been difficult to obtain. Here we devise an imaging approach to analyze mitochondrial translation within the context of single cells, by following the incorporation of clickable non‐canonical amino acids. We apply this method to multiple cell types, including specialized cells such as cardiomyocytes and neurons, and monitor with spatial resolution mitochondrial translation in axons and dendrites. We also show that translation imaging allows to monitor mitochondrial protein expression in patient fibroblasts. Approaching mitochondrial translation with click chemistry opens new avenues to understand how mitochondrial biogenesis is integrated into the cellular context and can be used to assess mitochondrial gene expression in mitochondrial diseases."],["dc.description.abstract","Synopsis image This study monitors mitochondrial protein synthesis with spatial resolution in single cells of multiple cell types. Labelling of mitochondrial translation products allows to monitor translation with spatial resolution within single cells. Mitochondria show different levels of protein synthesis within a single cell. Protein synthesis occurs in mitochondria of the pre‐ and the postsynapse."],["dc.description.abstract","This study monitors mitochondrial protein synthesis with spatial resolution in single cells of multiple cell types. image"],["dc.description.sponsorship","European Research Council (ERC) http://dx.doi.org/10.13039/501100000781"],["dc.description.sponsorship","Sonderforschungsbereiche (SFB)"],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft http://dx.doi.org/10.13039/501100001659"],["dc.description.sponsorship","Germany’s Excellence Strategy"],["dc.description.sponsorship","German Federal Ministry of Education and Research (BMBF)/DZHK"],["dc.description.sponsorship","Instituto de Salud Carlos III http://dx.doi.org/10.13039/501100004587"],["dc.description.sponsorship","Max Planck Institute for Biophysical Chemistry"],["dc.identifier.doi","10.15252/embr.202051635"],["dc.identifier.pmid","33586863"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82485"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/224"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/388"],["dc.identifier.url","https://sfb1286.uni-goettingen.de/literature/publications/107"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation","SFB 1286: Quantitative Synaptologie"],["dc.relation","SFB 1286 | A05: Mitochondriale Heterogenität in Synapsen"],["dc.relation","SFB 1286 | A06: Mitochondrienfunktion und -umsatz in Synapsen"],["dc.relation","SFB 1286 | Z03: Unkomplizierte multispektrale, superauflösende Bildgebung durch zehnfache Expansionsmikroskopie"],["dc.relation.eissn","1469-3178"],["dc.relation.issn","1469-221X"],["dc.relation.workinggroup","RG Jakobs (Structure and Dynamics of Mitochondria)"],["dc.relation.workinggroup","RG Rehling (Mitochondrial Protein Biogenesis)"],["dc.relation.workinggroup","RG Rizzoli (Quantitative Synaptology in Space and Time)"],["dc.relation.workinggroup","RG Cyganek (Stem Cell Unit)"],["dc.rights","This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs 4.0 License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made."],["dc.title","Monitoring mitochondrial translation in living cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","100026"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","STAR Protocols"],["dc.bibliographiccitation.volume","1"],["dc.contributor.author","Kleinsorge, Mandy"],["dc.contributor.author","Cyganek, Lukas"],["dc.date.accessioned","2022-05-13T09:51:16Z"],["dc.date.available","2022-05-13T09:51:16Z"],["dc.date.issued","2020"],["dc.description.abstract","The generation of homogeneous populations of subtype-specific cardiomyocytes derived from human induced pluripotent stem cells (hiPSCs) is crucial in cardiovascular disease modeling as well as in drug discovery and cardiotoxicity screenings. This protocol describes a simple, robust, and efficient monolayer-based differentiation of hiPSCs into defined atrial and ventricular cardiomyocytes. For complete details on the use and execution of this protocol, please refer to Cyganek et al., 2018."],["dc.identifier.doi","10.1016/j.xpro.2020.100026"],["dc.identifier.pmid","33111079"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/107867"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/356"],["dc.language.iso","en"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation","SFB 1002 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation.eissn","2666-1667"],["dc.relation.workinggroup","RG Cyganek (Stem Cell Unit)"],["dc.rights","CC BY-NC-ND 4.0"],["dc.title","Subtype-Directed Differentiation of Human iPSCs into Atrial and Ventricular Cardiomyocytes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","14689"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Sattler, Katherine"],["dc.contributor.author","El-Battrawy, Ibrahim"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Lang, Siegfried"],["dc.contributor.author","Lan, Huan"],["dc.contributor.author","Li, Xin"],["dc.contributor.author","Zhao, Zhihan"],["dc.contributor.author","Utikal, Jochen"],["dc.contributor.author","Wieland, Thomas"],["dc.contributor.author","Borggrefe, Martin"],["dc.contributor.author","Akin, Ibrahim"],["dc.date.accessioned","2021-09-01T06:42:20Z"],["dc.date.available","2021-09-01T06:42:20Z"],["dc.date.issued","2021"],["dc.description.abstract","Abstract The non-selective cation channel transient receptor potential vanilloid 1 (TRPV1) is expressed throughout the cardiovascular system. Recent evidence shows a role for TRPV1 in inflammatory processes. The role of TRPV1 for myocardial inflammation has not been established yet. Human induced pluripotent stem cell (iPSC)-derived cardiomyocytes (hiPSC-CM) from 4 healthy donors were incubated with lipopolysaccharides (LPS, 6 h), TRPV1 agonist capsaicin (CAP, 20 min) or the antagonist capsazepine (CPZ, 20 min). TRPV1 expression was studied by PCR and western blotting. TRPV1 internalization was analyzed by immunofluorescence. Interleukin-6 (IL-6) secretion and phosphorylation of JNK, p38 and ERK were determined by ELISA. TRPV1-associated ion channel current was measured by patch clamp. TRPV1-mRNA and -protein were expressed in hiPSC-CM. TRPV1 was localized in the plasma membrane. LPS significantly increased secretion of IL-6 by 2.3-fold, which was prevented by pre-incubation with CPZ. LPS induced TRPV1 internalization. Phosphorylation levels of ERK, p38 or JNK were not altered by TRPV1 stimulation or inhibition. LPS and IL-6 significantly lowered TRPV1-mediated ion channel current. TRPV1 mediates the LPS-induced inflammation in cardiomyocytes, associated with changes of cellular electrophysiology. LPS-induced inflammation results in TRPV1 internalization. Further studies have to examine the underlying pathways and the clinical relevance of these findings."],["dc.identifier.doi","10.1038/s41598-021-93958-3"],["dc.identifier.pii","93958"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/89034"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/399"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-455"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation.eissn","2045-2322"],["dc.relation.workinggroup","RG Cyganek (Stem Cell Unit)"],["dc.rights","CC BY 4.0"],["dc.title","TRPV1 activation and internalization is part of the LPS-induced inflammation in human iPSC-derived cardiomyocytes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]