Vettel, Christiane

[["dc.bibliographiccitation.firstpage","4865"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","The FASEB Journal"],["dc.bibliographiccitation.lastpage","4876"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Wuertz, Christina M."],["dc.contributor.author","Lorincz, Akos"],["dc.contributor.author","Vettel, Christiane"],["dc.contributor.author","Thomas, Martin A."],["dc.contributor.author","Wieland, Thomas"],["dc.contributor.author","Lutz, Susanne"],["dc.date.accessioned","2018-11-07T08:36:13Z"],["dc.date.available","2018-11-07T08:36:13Z"],["dc.date.issued","2010"],["dc.description.abstract","The purpose of our study was to investigate the role of endogenous p63RhoGEF in G(q/11)-dependent RhoA activation and signaling in rat aortic smooth muscle cells (RASMCs). Therefore, we studied the expression and subcellular localization in freshly isolated RASMCs and performed loss of function experiments to analyze its contribution to RhoGTPase activation and functional responses such as proliferation and contraction. By this, we could show that p63RhoGEF is endogenously expressed in RASMCs and acts there as the dominant mediator of the fast angiotensin II (ANG II)-dependent but not of the sphingosine-1-phosphate (S1P)-dependent RhoA activation. p63RhoGEF is not an activator of the concomitant Rac1 activation and functions independently of caveolae. The knockdown of endogenous p63RhoGEF significantly reduced the mitogenic response of ANG II, abolished ANG II-induced stress fiber formation and cell elongation in 2-D culture, and impaired the ANG II-driven contraction in a collagen-based 3-D model. In conclusion, our data provide for the first time evidence that p63RhoGEF is an important mediator of ANG II-dependent RhoA activation in RASMCs and therewith a leading actor in the subsequently triggered cellular processes, such as proliferation and contraction.-Wuertz, C. M., Lorincz, A., Vettel, C., Thomas, M. A., Wieland, T., Lutz, S. p63RhoGEF-a key mediator of angiotensin II-dependent signaling and processes in vascular smooth muscle cells. FASEB J. 24, 4865-4876 (2010). www.fasebj.org"],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft [Lu1486/1-1, SFB TR 23 TP B6]"],["dc.identifier.doi","10.1096/fj.10-155499"],["dc.identifier.isi","000284824400026"],["dc.identifier.pmid","20739613"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6271"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18258"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Federation Amer Soc Exp Biol"],["dc.relation.issn","0892-6638"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","p63RhoGEF-a key mediator of angiotensin II-dependent signaling and processes in vascular smooth muscle cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","15222"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Perera, Ruwan K."],["dc.contributor.author","Fischer, Thomas H."],["dc.contributor.author","Wagner, Michael"],["dc.contributor.author","Dewenter, Matthias"],["dc.contributor.author","Vettel, Christiane"],["dc.contributor.author","Bork, Nadja I."],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Conti, Marco"],["dc.contributor.author","Wess, Juergen"],["dc.contributor.author","El-Armouche, Ali"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Nikolaev, Viacheslav O."],["dc.date.accessioned","2018-04-23T11:48:02Z"],["dc.date.available","2018-04-23T11:48:02Z"],["dc.date.issued","2017"],["dc.description.abstract","Atropine is a clinically relevant anticholinergic drug, which blocks inhibitory effects of the parasympathetic neurotransmitter acetylcholine on heart rate leading to tachycardia. However, many cardiac effects of atropine cannot be adequately explained solely by its antagonism at muscarinic receptors. In isolated mouse ventricular cardiomyocytes expressing a Förster resonance energy transfer (FRET)-based cAMP biosensor, we confirmed that atropine inhibited acetylcholine-induced decreases in cAMP. Unexpectedly, even in the absence of acetylcholine, after G-protein inactivation with pertussis toxin or in myocytes from M2- or M1/3-muscarinic receptor knockout mice, atropine increased cAMP levels that were pre-elevated with the β-adrenergic agonist isoproterenol. Using the FRET approach and in vitro phosphodiesterase (PDE) activity assays, we show that atropine acts as an allosteric PDE type 4 (PDE4) inhibitor. In human atrial myocardium and in both intact wildtype and M2 or M1/3-receptor knockout mouse Langendorff hearts, atropine led to increased contractility and heart rates, respectively. In vivo, the atropine-dependent prolongation of heart rate increase was blunted in PDE4D but not in wildtype or PDE4B knockout mice. We propose that inhibition of PDE4 by atropine accounts, at least in part, for the induction of tachycardia and the arrhythmogenic potency of this drug."],["dc.identifier.doi","10.1038/s41598-017-15632-x"],["dc.identifier.gro","3142321"],["dc.identifier.pmid","29123207"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14861"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13454"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/194"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | D01: Erholung aus der Herzinsuffizienz – Einfluss von Fibrose und Transkriptionssignatur"],["dc.relation.issn","2045-2322"],["dc.relation.workinggroup","RG El-Armouche"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG L. Maier (Experimentelle Kardiologie)"],["dc.relation.workinggroup","RG Nikolaev (Cardiovascular Research Center)"],["dc.relation.workinggroup","RG T. Fischer"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Atropine augments cardiac contractility by inhibiting cAMP-specific phosphodiesterase type 4"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1763"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Pflügers Archiv - European Journal of Physiology"],["dc.bibliographiccitation.lastpage","1773"],["dc.bibliographiccitation.volume","465"],["dc.contributor.author","Schwoerer, A. P."],["dc.contributor.author","Neef, S."],["dc.contributor.author","Broichhausen, I."],["dc.contributor.author","Jacubeit, J."],["dc.contributor.author","Tiburcy, M."],["dc.contributor.author","Wagner, M."],["dc.contributor.author","Biermann, D."],["dc.contributor.author","Didié, M."],["dc.contributor.author","Vettel, C."],["dc.contributor.author","Maier, L. S."],["dc.contributor.author","Zimmermann, W. H."],["dc.contributor.author","Carrier, L."],["dc.contributor.author","Eschenhagen, T."],["dc.contributor.author","Volk, T."],["dc.contributor.author","El-Armouche, A."],["dc.contributor.author","Ehmke, H."],["dc.date.accessioned","2017-09-07T11:47:02Z"],["dc.date.available","2017-09-07T11:47:02Z"],["dc.date.issued","2013"],["dc.description.abstract","Cardiac atrophy as a consequence of mechanical unloading develops following exposure to microgravity or prolonged bed rest. It also plays a central role in the reverse remodelling induced by left ventricular unloading in patients with heart failure. Surprisingly, the intracellular Ca2+ transients which are pivotal to electromechanical coupling and to cardiac plasticity were repeatedly found to remain unaffected in early cardiac atrophy. To elucidate the mechanisms underlying the preservation of the Ca2+ transients, we investigated Ca2+ cycling in cardiomyocytes from mechanically unloaded (heterotopic abdominal heart transplantation) and control (orthotopic) hearts in syngeneic Lewis rats. Following 2 weeks of unloading, sarcoplasmic reticulum (SR) Ca2+ content was reduced by similar to 55 %. Atrophic cardiac myocytes also showed a much lower frequency of spontaneous diastolic Ca2+ sparks and a diminished systolic Ca2+ release, even though the expression of ryanodine receptors was increased by similar to 30 %. In contrast, current clamp recordings revealed prolonged action potentials in endocardial as well as epicardial myocytes which were associated with a two to fourfold higher sarcolemmal Ca2+ influx under action potential clamp. In addition, Cav1.2 subunits which form the pore of L-type Ca2+ channels (LTCC) were upregulated in atrophic myocardium. These data suggest that in early cardiac atrophy induced by mechanical unloading, an augmented sarcolemmal Ca2+ influx through LTCC fully compensates for a reduced systolic SR Ca2+ release to preserve the Ca2+ transient. This interplay involves an electrophysiological remodelling as well as changes in the expression of cardiac ion channels."],["dc.identifier.doi","10.1007/s00424-013-1316-y"],["dc.identifier.gro","3142244"],["dc.identifier.isi","000327409000009"],["dc.identifier.pmid","23842739"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10313"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/6132"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/54"],["dc.language.iso","en"],["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 | A02: Bedeutung des Phosphatase-Inhibitors-1 für die SR-spezifische Modulation der Beta- adrenozeptor-Signalkaskade"],["dc.relation","SFB 1002 | A03: Bedeutung CaMKII-abhängiger Mechanismen für die Arrhythmogenese bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation.eissn","1432-2013"],["dc.relation.issn","0031-6768"],["dc.relation.workinggroup","RG El-Armouche"],["dc.relation.workinggroup","RG L. Maier (Experimentelle Kardiologie)"],["dc.relation.workinggroup","RG Tiburcy (Stem Cell Disease Modeling)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Enhanced Ca2+ influx through cardiac L-type Ca2+ channels maintains the systolic Ca2+ transient in early cardiac atrophy induced by mechanical unloading"],["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"]]