Swain, Lija

[["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","603"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Antioxidants & Redox Signaling"],["dc.bibliographiccitation.lastpage","612"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Swain, Lija"],["dc.contributor.author","Nanadikar, Maithily S."],["dc.contributor.author","Borowik, Sergej"],["dc.contributor.author","Zieseniss, Anke"],["dc.contributor.author","Katschinski, Dörthe M."],["dc.date.accessioned","2020-12-10T18:16:01Z"],["dc.date.available","2020-12-10T18:16:01Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1089/ars.2017.7469"],["dc.identifier.eissn","1557-7716"],["dc.identifier.issn","1523-0864"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/75025"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Transgenic Organisms Meet Redox Bioimaging: One Step Closer to Physiology"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e2976"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Cell Death & Disease"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Beneke, Angelika"],["dc.contributor.author","Guentsch, Annemarie"],["dc.contributor.author","Hillemann, Annette"],["dc.contributor.author","Zieseniss, Anke"],["dc.contributor.author","Swain, Lija"],["dc.contributor.author","Katschinski, Dörthe M."],["dc.date.accessioned","2019-02-14T11:48:34Z"],["dc.date.available","2019-02-14T11:48:34Z"],["dc.date.issued","2017"],["dc.description.abstract","Macrophages are essential for the inflammatory response after an ischemic insult and thereby influence tissue recovery. For the oxygen sensing prolyl-4-hydroxylase domain enzyme (PHD) 2 a clear impact on the macrophage-mediated arteriogenic response after hind-limb ischemia has been demonstrated previously, which involves fine tuning a M2-like macrophage population. To analyze the role of PHD3 in macrophages, we performed hind-limb ischemia (ligation and excision of the femoral artery) in myeloid-specific PHD3 knockout mice (PHD3-/-) and analyzed the inflammatory cell invasion, reperfusion recovery and fibrosis in the ischemic muscle post-surgery. In contrast to PHD2, reperfusion recovery and angiogenesis was unaltered in PHD3-/- compared to WT mice. Macrophages from PHD3-/- mice showed, however, a dampened inflammatory reaction in the affected skeletal muscle tissues compared to WT controls. This was associated with a decrease in fibrosis and an anti-inflammatory phenotype of the PHD3-/- macrophages, as well as decreased expression of Cyp2s1 and increased PGE2-secretion, which could be mimicked by PHD3-/- bone marrow-derived macrophages in serum starvation."],["dc.identifier.doi","10.1038/cddis.2017.375"],["dc.identifier.pmid","28796258"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16494"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57561"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.eissn","2041-4889"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Loss of PHD3 in myeloid cells dampens the inflammatory response and fibrosis after hind-limb ischemia"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Acta Physiologica"],["dc.bibliographiccitation.volume","210"],["dc.contributor.author","Peters, J."],["dc.contributor.author","Vogler, Melanie"],["dc.contributor.author","Vogel, S."],["dc.contributor.author","Krull, Sabine"],["dc.contributor.author","Swain, Lija"],["dc.contributor.author","Katschinski, Doerthe Magdalena"],["dc.contributor.author","Zieseniss, Anke"],["dc.date.accessioned","2018-11-07T09:42:48Z"],["dc.date.available","2018-11-07T09:42:48Z"],["dc.date.issued","2014"],["dc.format.extent","130"],["dc.identifier.isi","000332259900335"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34038"],["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","Remodeling of the actin cytoskeleton in hypoxia: An emerging role for ArhGAP29"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]