Jatho, Aline

[["dc.bibliographiccitation.journal","Acta Physiologica"],["dc.bibliographiccitation.volume","216"],["dc.contributor.author","Jatho, Aline"],["dc.contributor.author","Hartmann, S."],["dc.contributor.author","Kittana, Naim"],["dc.contributor.author","Muegge, F."],["dc.contributor.author","Wuertz, Christina"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Katschinski, Doerthe Magdalena"],["dc.contributor.author","Lutz, S."],["dc.date.accessioned","2018-11-07T10:17:27Z"],["dc.date.available","2018-11-07T10:17:27Z"],["dc.date.issued","2016"],["dc.identifier.isi","000372285400124"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41230"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.issn","1748-1716"],["dc.relation.issn","1748-1708"],["dc.title","RhoA ambivalently controls prominent myofibroblast characteristics by involving distinct signaling routes"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Acta Physiologica"],["dc.bibliographiccitation.volume","213"],["dc.contributor.author","Jatho, Aline"],["dc.contributor.author","Kittana, Naim"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Lutz, S."],["dc.date.accessioned","2018-11-07T09:59:52Z"],["dc.date.available","2018-11-07T09:59:52Z"],["dc.date.issued","2015"],["dc.format.extent","115"],["dc.identifier.isi","000362554200255"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37688"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.issn","1748-1716"],["dc.relation.issn","1748-1708"],["dc.title","RhoA controls myofibroblast characteristics"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","39"],["dc.bibliographiccitation.journal","Journal of Molecular and Cellular Cardiology"],["dc.bibliographiccitation.lastpage","54"],["dc.bibliographiccitation.volume","88"],["dc.contributor.author","Ongherth, Anita"],["dc.contributor.author","Pasch, Sebastian"],["dc.contributor.author","Wuertz, Christina M."],["dc.contributor.author","Nowak, Karolin"],["dc.contributor.author","Kittana, Naim"],["dc.contributor.author","Weis, Cleo A."],["dc.contributor.author","Jatho, Aline"],["dc.contributor.author","Vettel, Christiane"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Wieland, Thomas"],["dc.contributor.author","Lutz, Susanne"],["dc.date.accessioned","2017-09-07T11:43:27Z"],["dc.date.available","2017-09-07T11:43:27Z"],["dc.date.issued","2015"],["dc.description.abstract","Cardiac remodeling, a hallmark of heart disease, is associated with intense auto- and paracrine signaling leading to cardiac fibrosis. We hypothesized that the specific mediator of G(q/11)-dependent RhoA activation p63RhoGEF, which is expressed in cardiac fibroblasts, plays a role in the underlying processes. We could show that p63RhoGEF is up-regulated in mouse hearts subjected to transverse aortic constriction (TAC). In an engineered heart muscle model (EHM), p63RhoGEF expression in cardiac fibroblasts increased resting and twitch tensions, and the dominant negative p63 Delta N decreased both. In an engineered connective tissue model (ECT), p63RhoGEF increased tissue stiffness and its knockdown as well as p63 Delta N reduced stiffness. In 2D cultures of neonatal rat cardiac fibroblasts, p63RhoGEF regulated the angiotensin II (Ang II)-dependent RhoA activation, the activation of the serum response factor, and the expression and secretion of the connective tissue growth factor (CTGF). All these processes were inhibited by the knockdown of p63RhoGEF or by p63 Delta N likely based on their negative influence on the actin cytoskeleton. Moreover, we show that p63RhoGEF also regulates CTGF in engineered tissues and correlates with it in the TAC model. Finally, confocal studies revealed a closely related localization of p63RhoGEF and CTGF in the trans-Golgi network. (C) 2015 Published by Elsevier Ltd."],["dc.identifier.doi","10.1016/j.yjmcc.2015.09.009"],["dc.identifier.gro","3141795"],["dc.identifier.isi","000365059300004"],["dc.identifier.pmid","26392029"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1157"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/117"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C02: RhoGTPasen und ihre Bedeutung für die Last-abhängige Myokardfibrose"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation.eissn","1095-8584"],["dc.relation.issn","0022-2828"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Lutz (G Protein-Coupled Receptor Mediated Signaling)"],["dc.relation.workinggroup","RG Tiburcy (Stem Cell Disease Modeling)"],["dc.relation.workinggroup","RG Toischer (Kardiales Remodeling)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.title","p63RhoGEF regulates auto- and paracrine signaling in cardiac fibroblasts"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Naunyn-Schmiedeberg s Archives of Pharmacology"],["dc.bibliographiccitation.volume","389"],["dc.contributor.author","Hartmann, S."],["dc.contributor.author","Jatho, Aline"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Ridley, Anna R."],["dc.contributor.author","Lutz, S."],["dc.date.accessioned","2018-11-07T10:19:00Z"],["dc.date.available","2018-11-07T10:19:00Z"],["dc.date.issued","2016"],["dc.format.extent","S35"],["dc.identifier.isi","000398368200142"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41569"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.conference","82nd Annual Meeting of the German-Society-for-Exerimental-and-Clinical-Pharmacology-and-Toxicology (DGPT) / 18th Annual Meeting of the Network-Clinical-Pharmacology-Germany (VKliPha)"],["dc.relation.eventlocation","Berlin, GERMANY"],["dc.relation.issn","1432-1912"],["dc.relation.issn","0028-1298"],["dc.title","Rho-associated kinases ROCK1 and ROCK2 affect myofibroblast characteristics of cardiac fibroblasts"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","843"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Cellular Physiology and Biochemistry"],["dc.bibliographiccitation.lastpage","851"],["dc.bibliographiccitation.volume","36"],["dc.contributor.author","Zieseniss, Anke"],["dc.contributor.author","Hesse, Amke Rena"],["dc.contributor.author","Jatho, Aline"],["dc.contributor.author","Krull, Sabine"],["dc.contributor.author","Hoelscher, Marion"],["dc.contributor.author","Vogel, Sabine"],["dc.contributor.author","Katschinski, Doerthe Magdalena"],["dc.date.accessioned","2018-11-07T10:03:08Z"],["dc.date.available","2018-11-07T10:03:08Z"],["dc.date.issued","2015"],["dc.description.abstract","Aims: The prolyl-4-hydroxylase domain (PHD) enzymes are representing novel therapeutic targets for ischemic tissue protection. Whereas the consequences of a knock out of the PHDs have been analyzed in the context of cardioprotection, the implications of PHD overexpression is unknown so far. Methods and Results: We generated cardiomyocyte-specific PHD3 transgenic mice (cPhd3tg). Resting cPhd3tg mice did not show constitutive accumulation of HIF-l alpha or HIF-2 alpha or changes in HIF target gene expression in the heart. Cardiac function was followed up for 14 months in these mice and found to be unchanged. After challenging the cPhd3tg mice with ligation of the left anterior descending artery, HIF-1 alpha/-2 alpha accumulation in the left ventricles was blunted. This was associated with a significantly increased infarct size of the cPhd3tg compared to wild type mice. Conclusion: Whereas overexpression of PHD3 in the resting state does not significantly influence cardiac function, it is crucial for the cardiac response to ischemia by affecting HIF alpha accumulation in the ischemic tissue. Copyright (C) 2015 S Karger AG, Basel"],["dc.description.sponsorship","Deutsche Zentrum fur Herz Kreislaufforschung (DZHK)"],["dc.identifier.doi","10.1159/000430260"],["dc.identifier.isi","000357833400002"],["dc.identifier.pmid","26044310"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38386"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","1421-9778"],["dc.relation.issn","1015-8987"],["dc.title","Cardiomyocyte-Specific Transgenic Expression of Prolyl-4-Hydroxylase Domain 3 Impairs the Myocardial Response to Ischemia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1705"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Current Psychology"],["dc.bibliographiccitation.lastpage","1714"],["dc.bibliographiccitation.volume","39"],["dc.contributor.author","Basilowski, M."],["dc.contributor.author","Schönfeld, B."],["dc.contributor.author","Esser, S."],["dc.contributor.author","Jatho, A."],["dc.contributor.author","Kownatka, M."],["dc.contributor.author","Signerski-Krieger, J."],["dc.contributor.author","Esselmann, H."],["dc.contributor.author","Grabemann, M."],["dc.contributor.author","Mette, C."],["dc.contributor.author","Strunz, L."],["dc.contributor.author","Zimmermann, M."],["dc.contributor.author","Lajcsak, E."],["dc.contributor.author","Scherbaum, N."],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Kis, B."],["dc.contributor.author","Abdel-Hamid, M."],["dc.date.accessioned","2021-04-14T08:23:33Z"],["dc.date.available","2021-04-14T08:23:33Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1007/s12144-018-9868-9"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/80961"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1936-4733"],["dc.relation.issn","1046-1310"],["dc.title","From Bones to Brain: 50 Years of Star Trek and Changes in the Stigmatization of Psychological Disorders"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Naunyn-Schmiedeberg s Archives of Pharmacology"],["dc.bibliographiccitation.volume","388"],["dc.contributor.author","Weber, P."],["dc.contributor.author","Baltus, D."],["dc.contributor.author","Jatho, Aline"],["dc.contributor.author","Zelarayan-Behrend, L."],["dc.contributor.author","Lutz, S."],["dc.contributor.author","Wieland, Thomas"],["dc.date.accessioned","2018-11-07T10:01:11Z"],["dc.date.available","2018-11-07T10:01:11Z"],["dc.date.issued","2015"],["dc.format.extent","S12"],["dc.identifier.isi","000359539100042"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37960"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.eventlocation","Kiel, GERMANY"],["dc.relation.issn","1432-1912"],["dc.relation.issn","0028-1298"],["dc.title","RhoGEF17 stabilizes the adherens junction complex of endothelial cells"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Naunyn-Schmiedeberg s Archives of Pharmacology"],["dc.bibliographiccitation.volume","386"],["dc.contributor.author","Jatho, Aline"],["dc.contributor.author","Kittana, Naim"],["dc.contributor.author","Schenk, K."],["dc.contributor.author","Ramba, Beate"],["dc.contributor.author","Chaponnier, C."],["dc.contributor.author","Wuertz, Christina"],["dc.contributor.author","Lutz, S."],["dc.date.accessioned","2018-11-07T09:28:54Z"],["dc.date.available","2018-11-07T09:28:54Z"],["dc.date.issued","2013"],["dc.format.extent","S38"],["dc.identifier.isi","000209476400147"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30896"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.issn","1432-1912"],["dc.relation.issn","0028-1298"],["dc.title","RhoA regulates cytoskeletal composition, integrity and dynamics and thus influences movement-related processes in cardiac fibroblasts"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Naunyn-Schmiedeberg s Archives of Pharmacology"],["dc.bibliographiccitation.volume","385"],["dc.contributor.author","Jatho, Aline"],["dc.contributor.author","Zieseniss, Anke"],["dc.contributor.author","Schenk, K."],["dc.contributor.author","Ramba, Beate"],["dc.contributor.author","Wuertz, Christina"],["dc.contributor.author","Lutz, S."],["dc.date.accessioned","2018-11-07T09:12:58Z"],["dc.date.available","2018-11-07T09:12:58Z"],["dc.date.issued","2012"],["dc.format.extent","42"],["dc.identifier.isi","000300779500179"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27066"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.conference","78th Annual Congress of the German-Society-for-Experimental-and-Clinical-Pharmacology-and-Toxicology (DGPT)"],["dc.relation.eventlocation","Dresden, GERMANY"],["dc.relation.issn","0028-1298"],["dc.title","RhoA influences adhesion and spreading of cardiac fibroblasts via complex regulation of cytoskeletal proteins"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1004"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Circulation Research"],["dc.bibliographiccitation.lastpage","1016"],["dc.bibliographiccitation.volume","119"],["dc.contributor.author","Swain, Lija"],["dc.contributor.author","Kesemeyer, Andrea"],["dc.contributor.author","Meyer-Roxlau, Stefanie"],["dc.contributor.author","Vettel, Christiane"],["dc.contributor.author","Zieseniss, Anke"],["dc.contributor.author","Güntsch, Annemarie"],["dc.contributor.author","Jatho, Aline"],["dc.contributor.author","Becker, Andreas"],["dc.contributor.author","Nanadikar, Maithily S."],["dc.contributor.author","Morgan, Bruce"],["dc.contributor.author","Dennerlein, Sven"],["dc.contributor.author","Shah, Ajay M."],["dc.contributor.author","El-Armouche, Ali"],["dc.contributor.author","Nikolaev, Viacheslav O."],["dc.contributor.author","Katschinski, Dörthe M."],["dc.date.accessioned","2020-12-10T18:37:59Z"],["dc.date.available","2020-12-10T18:37:59Z"],["dc.date.issued","2016"],["dc.description.abstract","Rationale: Changes in redox potentials of cardiac myocytes are linked to several cardiovascular diseases. Redox alterations are currently mostly described qualitatively using chemical sensors, which however do not allow quantifying redox potentials, lack specificity, and the possibility to analyze subcellular domains. Recent advances to quantitatively describe defined redox changes include the application of genetically encoded redox biosensors. Objective: Establishment of mouse models, which allow the quantification of the glutathione redox potential (E-GSH) in the cytoplasm and the mitochondrial matrix of isolated cardiac myocytes and in Langendorff-perfused hearts based on the use of the redox-sensitive green fluorescent protein 2, coupled to the glutaredoxin 1 (Grx1-roGFP2). Methods and Results: We generated transgenic mice with cardiac myocyte-restricted expression of Grx1-roGFP2 targeted either to the mitochondrial matrix or to the cytoplasm. The response of the roGFP2 toward H2O2, diamide, and dithiothreitol was titrated and used to determine the E-GSH in isolated cardiac myocytes and in Langendorff-perfused hearts. Distinct E-GSH were observed in the cytoplasm and the mitochondrial matrix. Stimulation of the cardiac myocytes with isoprenaline, angiotensin II, or exposure to hypoxia/reoxygenation additionally underscored that these compartments responded independently. A compartment-specific response was also observed 3 to 14 days after myocardial infarction. Conclusions: We introduce redox biosensor mice as a new tool, which allows quantification of defined alterations of E-GSH in the cytoplasm and the mitochondrial matrix in cardiac myocytes and can be exploited to answer questions in basic and translational cardiovascular research."],["dc.identifier.doi","10.1161/CIRCRESAHA.116.309551"],["dc.identifier.eissn","1524-4571"],["dc.identifier.isi","000386313900013"],["dc.identifier.issn","0009-7330"],["dc.identifier.pmid","27553648"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77158"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","1524-4571"],["dc.relation.issn","0009-7330"],["dc.title","Redox Imaging Using Cardiac Myocyte-Specific Transgenic Biosensor Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]