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","741"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Cells"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Weber, Pamina"],["dc.contributor.author","Baltus, Doris"],["dc.contributor.author","Jatho, Aline"],["dc.contributor.author","Drews, Oliver"],["dc.contributor.author","Zelarayan, Laura C."],["dc.contributor.author","Wieland, Thomas"],["dc.contributor.author","Lutz, Susanne"],["dc.date.accessioned","2021-06-01T09:42:32Z"],["dc.date.available","2021-06-01T09:42:32Z"],["dc.date.issued","2021"],["dc.description.abstract","The Rho guanine nucleotide exchange factor RhoGEF17 was described to reside in adherens junctions (AJ) in endothelial cells (EC) and to play a critical role in the regulation of cell adhesion and barrier function. The purpose of this study was to analyze signal cascades and processes occurring subsequent to AJ disruption induced by RhoGEF17 knockdown. Primary human and immortalized rat EC were used to demonstrate that an adenoviral-mediated knockdown of RhoGEF17 resulted in cell rounding and an impairment in spheroid formation due to an enhanced proteasomal degradation of AJ components. In contrast, β-catenin degradation was impaired, which resulted in an induction of the β-catenin-target genes cyclin D1 and survivin. RhoGEF17 depletion additionally inhibited cell adhesion and sheet migration. The RhoGEF17 knockdown prevented the cells with impeded cell–cell and cell–matrix contacts from apoptosis, which was in line with a reduction in pro-caspase 3 expression and an increase in Akt phosphorylation. Nevertheless, the cells were not able to proliferate as a cell cycle block occurred. In summary, we demonstrate that a loss of RhoGEF17 disturbs cell–cell and cell–substrate interaction in EC. Moreover, it prevents the EC from cell death and blocks cell proliferation. Non-canonical β-catenin signaling and Akt activation could be identified as a potential mechanism."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft"],["dc.identifier.doi","10.3390/cells10040741"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85279"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/391"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C02: RhoGTPasen und ihre Bedeutung für die Last-abhängige Myokardfibrose"],["dc.relation.eissn","2073-4409"],["dc.relation.workinggroup","RG Lutz (G Protein-Coupled Receptor Mediated Signaling)"],["dc.relation.workinggroup","RG Zelarayán-Behrend (Developmental Pharmacology)"],["dc.rights","https://creativecommons.org/licenses/by/4.0/"],["dc.title","RhoGEF17—An Essential Regulator of Endothelial Cell Death and Growth"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0137519"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Jatho, Aline"],["dc.contributor.author","Hartmann, Svenja"],["dc.contributor.author","Kittana, Naim"],["dc.contributor.author","Muegge, Felicitas"],["dc.contributor.author","Wuertz, Christina M."],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Katschinski, Dörthe M."],["dc.contributor.author","Lutz, Susanne"],["dc.date.accessioned","2017-09-07T11:43:28Z"],["dc.date.available","2017-09-07T11:43:28Z"],["dc.date.issued","2015"],["dc.description.abstract","Introduction RhoA has been shown to be beneficial in cardiac disease models when overexpressed in cardiomyocytes, whereas its role in cardiac fibroblasts (CF) is still poorly understood. During cardiac remodeling CF undergo a transition towards a myofibroblast phenotype thereby showing an increased proliferation and migration rate. Both processes involve the remodeling of the cytoskeleton. Since RhoA is known to be a major regulator of the cytoskeleton, we analyzed its role in CF and its effect on myofibroblast characteristics in 2 D and 3D models. Results Downregulation of RhoA was shown to strongly affect the actin cytoskeleton. It decreased the myofibroblast marker alpha-sm-actin, but increased certain fibrosis-associated factors like TGF-beta and collagens. Also, the detailed analysis of CTGF expression demonstrated that the outcome of RhoA signaling strongly depends on the involved stimulus. Furthermore, we show that proliferation of myofibroblasts rely on RhoA and tubulin acetylation. In assays accessing three different types of migration, we demonstrate that RhoA/ROCK/Dia1 are important for 2D migration and the repression of RhoA and Dia1 signaling accelerates 3D migration. Finally, we show that a downregulation of RhoA in CF impacts the viscoelastic and contractile properties of engineered tissues. Conclusion RhoA positively and negatively influences myofibroblast characteristics by differential signaling cascades and depending on environmental conditions. These include gene expression, migration and proliferation. Reduction of RhoA leads to an increased viscoelasticity and a decrease in contractile force in engineered cardiac tissue."],["dc.description.sponsorship","Open-Access Publikationsfonds 2015"],["dc.identifier.doi","10.1371/journal.pone.0137519"],["dc.identifier.gro","3141809"],["dc.identifier.isi","000362511000003"],["dc.identifier.pmid","26448568"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12214"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1312"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/118"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["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","SFB 1002 | C06: Mechanismen und Regulation der koronaren Gefäßneubildung"],["dc.relation.issn","1932-6203"],["dc.relation.workinggroup","RG Lutz (G Protein-Coupled Receptor Mediated Signaling)"],["dc.relation.workinggroup","RG Tiburcy (Stem Cell Disease Modeling)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","RhoA Ambivalently Controls Prominent Myofibroblast Characteritics by Involving Distinct Signaling Routes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["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"]]