Lutz, Susanne

[["dc.bibliographiccitation.firstpage","6427"],["dc.bibliographiccitation.journal","International Journal of Nanomedicine"],["dc.bibliographiccitation.lastpage","6428"],["dc.bibliographiccitation.volume","Volume 16"],["dc.contributor.author","Kittana, Naim"],["dc.contributor.author","Assali, Mohyeddin"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Liaw, Norman"],["dc.contributor.author","Santos, Gabriela Leao"],["dc.contributor.author","Rehman, Abdul"],["dc.contributor.author","Lutz, Susanne"],["dc.date.accessioned","2022-06-08T07:57:29Z"],["dc.date.available","2022-06-08T07:57:29Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.2147/IJN.S339659"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/110104"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-575"],["dc.relation.eissn","1178-2013"],["dc.title","Modulating the Biomechanical Properties of Engineered Connective Tissues by Chitosan-Coated Multiwall Carbon Nanotubes [Corrigendum]"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","31"],["dc.bibliographiccitation.journal","Journal of Molecular and Cellular Cardiology"],["dc.bibliographiccitation.lastpage","43"],["dc.bibliographiccitation.volume","127"],["dc.contributor.author","Morhenn, Karoline"],["dc.contributor.author","Quentin, Thomas"],["dc.contributor.author","Wichmann, Helen"],["dc.contributor.author","Steinmetz, Michael"],["dc.contributor.author","Prondzynski, Maksymilian"],["dc.contributor.author","Söhren, Klaus-Dieter"],["dc.contributor.author","Christ, Torsten"],["dc.contributor.author","Geertz, Birgit"],["dc.contributor.author","Schröder, Sabine"],["dc.contributor.author","Schöndube, Friedrich A."],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Schlossarek, Saskia"],["dc.contributor.author","Zimmermann, Wolfram H."],["dc.contributor.author","Carrier, Lucie"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.contributor.author","Cardinaux, Jean-René"],["dc.contributor.author","Lutz, Susanne"],["dc.contributor.author","Oetjen, Elke"],["dc.date.accessioned","2020-12-10T15:21:48Z"],["dc.date.available","2020-12-10T15:21:48Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1016/j.yjmcc.2018.12.001"],["dc.identifier.issn","0022-2828"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73167"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Mechanistic role of the CREB-regulated transcription coactivator 1 in cardiac hypertrophy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["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","1596"],["dc.bibliographiccitation.issue","17"],["dc.bibliographiccitation.journal","Journal of the American College of Cardiology"],["dc.bibliographiccitation.lastpage","1606"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Mehel, Hind"],["dc.contributor.author","Emons, Julius"],["dc.contributor.author","Vettel, Christiane"],["dc.contributor.author","Wittköpper, Katrin"],["dc.contributor.author","Seppelt, Danilo"],["dc.contributor.author","Dewenter, Matthias"],["dc.contributor.author","Lutz, Susanne"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Lechêne, Patrick"],["dc.contributor.author","Leroy, Jérôme"],["dc.contributor.author","Lefebvre, Florence"],["dc.contributor.author","Varin, Audrey"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.contributor.author","Nattel, Stanley"],["dc.contributor.author","Dobrev, Dobromir"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Nikolaev, Viacheslav O."],["dc.contributor.author","Vandecasteele, Grégoire"],["dc.contributor.author","Fischmeister, Rodolphe"],["dc.contributor.author","El-Armouche, Ali"],["dc.date.accessioned","2019-01-14T16:02:22Z"],["dc.date.available","2019-01-14T16:02:22Z"],["dc.date.issued","2013"],["dc.description.abstract","Objectives This study investigated whether myocardial phosphodiesterase-2 (PDE2) is altered in heart failure (HF) and determined PDE2-mediated effects on beta-adrenergic receptor (β-AR) signaling in healthy and diseased cardiomyocytes. Background Diminished cyclic adenosine monophosphate (cAMP) and augmented cyclic guanosine monophosphate (cGMP) signaling is characteristic for failing hearts. Among the PDE superfamily, PDE2 has the unique property of being able to be stimulated by cGMP, thus leading to a remarkable increase in cAMP hydrolysis mediating a negative cross talk between cGMP and cAMP signaling. However, the role of PDE2 in HF is poorly understood. Methods Immunoblotting, radioenzymatic- and fluorescence resonance energy transfer–based assays, video edge detection, epifluorescence microscopy, and L-type Ca2+ current measurements were performed in myocardial tissues and/or isolated cardiomyocytes from human and/or experimental HF, respectively. Results Myocardial PDE2 expression and activity were ∼2-fold higher in advanced human HF. Chronic β-AR stimulation via catecholamine infusions in rats enhanced PDE2 expression ∼2-fold and cAMP hydrolytic activity ∼4-fold, which correlated with blunted cardiac β-AR responsiveness. In diseased cardiomyocytes, higher PDE2 activity could be further enhanced by stimulation of cGMP synthesis via nitric oxide donors, whereas specific PDE2 inhibition partially restored β-AR responsiveness. Accordingly, PDE2 overexpression in healthy cardiomyocytes reduced the rise in cAMP levels and L-type Ca2+ current amplitude, and abolished the inotropic effect following acute β-AR stimulation, without affecting basal contractility. Importantly, PDE2-overexpressing cardiomyocytes showed marked protection from norepinephrine-induced hypertrophic responses. Conclusions PDE2 is markedly up-regulated in failing hearts and desensitizes against acute β-AR stimulation. This may constitute an important defense mechanism during cardiac stress, for example, by antagonizing excessive β-AR drive. Thus, activating myocardial PDE2 may represent a novel intracellular antiadrenergic therapeutic strategy in HF."],["dc.identifier.doi","10.1016/j.jacc.2013.05.057"],["dc.identifier.gro","3142269"],["dc.identifier.isi","000325937400010"],["dc.identifier.pmid","23810893"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57317"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/37"],["dc.language.iso","en"],["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 | A01: cAMP- und cGMP- Mikrodomänen bei Herzhypertrophie und Insuffizienz"],["dc.relation","SFB 1002 | A02: Bedeutung des Phosphatase-Inhibitors-1 für die SR-spezifische Modulation der Beta- adrenozeptor-Signalkaskade"],["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","1558-3597"],["dc.relation.issn","1558-3597"],["dc.relation.issn","0735-1097"],["dc.relation.workinggroup","RG El-Armouche"],["dc.relation.workinggroup","RG Lutz (G Protein-Coupled Receptor Mediated Signaling)"],["dc.relation.workinggroup","RG L. Maier (Experimentelle Kardiologie)"],["dc.relation.workinggroup","RG Nikolaev (Cardiovascular Research Center)"],["dc.relation.workinggroup","RG Sossalla (Kardiovaskuläre experimentelle Elektrophysiologie und Bildgebung)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.title","Phosphodiesterase-2 Is Up-Regulated in Human Failing Hearts and Blunts β-Adrenergic Responses in Cardiomyocytes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["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.firstpage","315"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.lastpage","327"],["dc.bibliographiccitation.volume","115"],["dc.contributor.author","Dworatzek, Elke"],["dc.contributor.author","Mahmoodzadeh, Shokoufeh"],["dc.contributor.author","Schriever, Cindy"],["dc.contributor.author","Kusumoto, Kana"],["dc.contributor.author","Kramer, Lisa"],["dc.contributor.author","Santos, Gabriela"],["dc.contributor.author","Fliegner, Daniela"],["dc.contributor.author","Leung, Yuet-Kin"],["dc.contributor.author","Ho, Shuk-Mei"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Lutz, Susanne"],["dc.contributor.author","Regitz-Zagrosek, Vera"],["dc.date.accessioned","2020-12-10T18:18:49Z"],["dc.date.available","2020-12-10T18:18:49Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1093/cvr/cvy185"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/75099"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/293"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["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.workinggroup","RG Lutz (G Protein-Coupled Receptor Mediated Signaling)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.title","Sex-specific regulation of collagen I and III expression by 17β-Estradiol in cardiac fibroblasts: role of estrogen receptors"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","174"],["dc.bibliographiccitation.journal","Journal of Visualized Experiments"],["dc.contributor.author","Santos, Gabriela L."],["dc.contributor.author","Meyer, Tim"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","DeGrave, Alisa"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Lutz, Susanne"],["dc.date.accessioned","2021-12-01T09:22:54Z"],["dc.date.available","2021-12-01T09:22:54Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.3791/62700"],["dc.identifier.pmid","34487119"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94508"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/338"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/402"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["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","1940-087X"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.relation.workinggroup","RG Lutz (G Protein-Coupled Receptor Mediated Signaling)"],["dc.relation.workinggroup","RG Tiburcy (Stem Cell Disease Modeling)"],["dc.title","Fibroblast Derived Human Engineered Connective Tissue for Screening Applications"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","989"],["dc.bibliographiccitation.journal","International Journal of Nanomedicine"],["dc.bibliographiccitation.lastpage","1000"],["dc.bibliographiccitation.volume","Volume 16"],["dc.contributor.author","Kittana, Naim"],["dc.contributor.author","Assali, Mohyeddin"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Liaw, Norman"],["dc.contributor.author","Santos, Gabriela Leao"],["dc.contributor.author","Rehman, Abdul"],["dc.contributor.author","Lutz, Susanne"],["dc.date.accessioned","2021-04-14T08:29:53Z"],["dc.date.available","2021-04-14T08:29:53Z"],["dc.date.issued","2021"],["dc.description.abstract","Background: Under certain conditions, the physiological repair of connective tissues might fail to restore the original structure and function. Optimized engineered connective tissues (ECTs) with biophysical properties adapted to the target tissue could be used as a substitution therapy. This study aimed to investigate the effect of ECT enforcement by a complex of multiwall carbon nanotubes with chitosan (C-MWCNT) to meet in vivo demands.\r\nMaterials and Methods: ECTs were constructed from human foreskin fibroblasts (HFF-1) in collagen type I and enriched with the three different percentages 0.025, 0.05 and 0.1% of C-MWCNT. Characterization of the physical properties was performed by biomechanical studies using unidirectional strain.\r\nResults: Supplementation with 0.025% C-MWCNT moderately increased the tissue stiffness, reflected by Young’s modulus, compared to tissues without C-MWCNT. Supplementation of ECTs with 0.1% C-MWCNT reduced tissue contraction and increased the elasticity and the extensibility, reflected by the yield point and ultimate strain, respectively. Consequently, the ECTs with 0.1% C-MWCNT showed a higher resilience and toughness as control tissues. Fluorescence tissue imaging demonstrated the longitudinal alignment of all cells independent of the condition.\r\nConclusion: Supplementation with C-MWCNT can enhance the biophysical properties of ECTs, which could be advantageous for applications in connective tissue repair."],["dc.identifier.doi","10.2147/IJN.S289107"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83018"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/387"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["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","1178-2013"],["dc.relation.workinggroup","RG Lutz (G Protein-Coupled Receptor Mediated Signaling)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.rights","CC BY-NC 3.0"],["dc.title","Modulating the Biomechanical Properties of Engineered Connective Tissues by Chitosan-Coated Multiwall Carbon Nanotubes"],["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","H1246"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","American Journal of Physiology - Heart and Circulatory Physiology"],["dc.bibliographiccitation.lastpage","H1252"],["dc.bibliographiccitation.volume","306"],["dc.contributor.author","Vettel, C."],["dc.contributor.author","Lämmle, S."],["dc.contributor.author","Ewens, S."],["dc.contributor.author","Cervirgen, C."],["dc.contributor.author","Emmons, J."],["dc.contributor.author","Ongherth, A."],["dc.contributor.author","Dewenter, M."],["dc.contributor.author","Lindner, D."],["dc.contributor.author","Westermann, D."],["dc.contributor.author","Nikolaev, V. O."],["dc.contributor.author","Lutz, S."],["dc.contributor.author","Zimmermann, W.-H."],["dc.contributor.author","El-Armouche, A."],["dc.date.accessioned","2017-09-07T11:46:22Z"],["dc.date.available","2017-09-07T11:46:22Z"],["dc.date.issued","2014"],["dc.description.abstract","Recent studies suggest that the signal molecules cAMP and cGMP have antifibrotic effects by negatively regulating pathways associated with fibroblast to myofibroblast (MyoCF) conversion. The phosphodiesterase 2 (PDE2) has the unique property to be stimulated by cGMP, which leads to a remarkable increase in cAMP hydrolysis and thus mediates a negative cross-talk between both pathways. PDE2 has been recently investigated in cardiomyocytes; here we specifically addressed its role in fibroblast conversion and cardiac fibrosis. PDE2 is abundantly expressed in both neonatal rat cardiac fibroblasts (CFs) and cardiomyocytes. The overexpression of PDE2 in CFs strongly reduced basal and isoprenaline-induced cAMP synthesis, and this decrease was sufficient to induce MyoCF conversion even in the absence of exogenous profibrotic stimuli. Functional stress-strain experiments with fibroblast-derived engineered connective tissue (ECT) demonstrated higher stiffness in ECTs overexpressing PDE2. In regard to cGMP, neither basal nor atrial natriuretic peptide-induced cGMP levels were affected by PDE2, whereas the response to nitric oxide donor sodium nitroprusside was slightly but significantly reduced. Interestingly, despite persistently depressed cAMP levels, both cGMP-elevating stimuli were able to completely prevent the PDE2-induced MyoCF phenotype, arguing for a double-tracked mechanism. In conclusion, PDE2 accelerates CF to MyoCF conversion, which leads to greater stiffness in ECTs. Atrial natriuretic peptide-and sodium nitroprusside-mediated cGMP synthesis completely reverses PDE2-induced fibroblast conversion. Thus PDE2 may augment cardiac remodeling, but this effect can also be overcome by enhanced cGMP. The redundant role of cAMP and cGMP as antifibrotic meditators may be viewed as a protective mechanism in heart failure."],["dc.identifier.doi","10.1152/ajpheart.00852.2013"],["dc.identifier.gro","3142154"],["dc.identifier.isi","000334596500016"],["dc.identifier.pmid","24531807"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/5133"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/67"],["dc.language.iso","en"],["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 | A02: Bedeutung des Phosphatase-Inhibitors-1 für die SR-spezifische Modulation der Beta- adrenozeptor-Signalkaskade"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation.eissn","1522-1539"],["dc.relation.issn","0363-6135"],["dc.relation.workinggroup","RG El-Armouche"],["dc.relation.workinggroup","RG Lutz (G Protein-Coupled Receptor Mediated Signaling)"],["dc.relation.workinggroup","RG Nikolaev (Cardiovascular Research Center)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.title","PDE2-mediated cAMP hydrolysis accelerates cardiac fibroblast to myofibroblast conversion and is antagonized by exogenous activation of cGMP signaling pathways"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","13"],["dc.bibliographiccitation.journal","Journal of Molecular and Cellular Cardiology"],["dc.bibliographiccitation.lastpage","28"],["dc.bibliographiccitation.volume","134"],["dc.contributor.author","Santos, Gabriela Leão"],["dc.contributor.author","Hartmann, Svenja"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Ridley, Anne"],["dc.contributor.author","Lutz, Susanne"],["dc.date.accessioned","2020-12-10T15:21:48Z"],["dc.date.available","2020-12-10T15:21:48Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1016/j.yjmcc.2019.06.015"],["dc.identifier.pmid","31233754"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16472"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73169"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/304"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["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.workinggroup","RG Lutz (G Protein-Coupled Receptor Mediated Signaling)"],["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","Inhibition of Rho-associated kinases suppresses cardiac myofibroblast function in engineered connective and heart muscle tissues"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]