Jatho, Aline

[["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.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"]]

[["dc.bibliographiccitation.journal","Acta Physiologica"],["dc.bibliographiccitation.volume","219"],["dc.contributor.author","Swain, Lija"],["dc.contributor.author","Kesemeyer, Andrea"],["dc.contributor.author","Meyer-Roxlau, Stefanie"],["dc.contributor.author","Vettel, Christiane"],["dc.contributor.author","Glintsch, A."],["dc.contributor.author","Zieseniss, Anke"],["dc.contributor.author","Jatho, Aline"],["dc.contributor.author","Morgan, B."],["dc.contributor.author","Dennedein, S."],["dc.contributor.author","Shah, Ajay M."],["dc.contributor.author","Ali, E.-A."],["dc.contributor.author","Nikolaev, V."],["dc.contributor.author","Katschinski, Doerthe Magdalena"],["dc.date.accessioned","2018-11-07T10:26:38Z"],["dc.date.available","2018-11-07T10:26:38Z"],["dc.date.issued","2017"],["dc.identifier.isi","000395770300308"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43083"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Wiley"],["dc.publisher.place","Hoboken"],["dc.title","Generation and characterization of glutathione redox potential sensor mice"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1208"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Circulation Research"],["dc.bibliographiccitation.lastpage","1210"],["dc.bibliographiccitation.volume","128"],["dc.contributor.author","Jatho, Aline"],["dc.contributor.author","Zieseniss, Anke"],["dc.contributor.author","Brechtel-Curth, Katja"],["dc.contributor.author","Yamamoto, Atsushi"],["dc.contributor.author","Coleman, Mathew L."],["dc.contributor.author","Vergel Leon, Ana M."],["dc.contributor.author","Biggs, Daniel"],["dc.contributor.author","Davies, Ben"],["dc.contributor.author","Pugh, Chris W."],["dc.contributor.author","Katschinski, Dörthe M."],["dc.date.accessioned","2021-06-01T09:42:11Z"],["dc.date.available","2021-06-01T09:42:11Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1161/CIRCRESAHA.120.318216"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85170"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1524-4571"],["dc.relation.issn","0009-7330"],["dc.title","Precisely Tuned Inhibition of HIF Prolyl Hydroxylases Is Key for Cardioprotection After Ischemia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]