El-Armouche, Ali

[["dc.bibliographiccitation.firstpage","1270"],["dc.bibliographiccitation.issue","23"],["dc.bibliographiccitation.journal","DMW - Deutsche Medizinische Wochenschrift"],["dc.bibliographiccitation.lastpage","1274"],["dc.bibliographiccitation.volume","136"],["dc.contributor.author","Wittkoepper, Katrin"],["dc.contributor.author","Emons, J."],["dc.contributor.author","El-Armouche, Ali"],["dc.date.accessioned","2018-11-07T08:55:32Z"],["dc.date.available","2018-11-07T08:55:32Z"],["dc.date.issued","2011"],["dc.identifier.doi","10.1055/s-0031-1272573"],["dc.identifier.isi","000291091800009"],["dc.identifier.pmid","21607898"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22932"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.relation.issn","0012-0472"],["dc.title","Febuxostat"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","H533"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","American Journal of Physiology - Heart and Circulatory Physiology"],["dc.bibliographiccitation.lastpage","H541"],["dc.bibliographiccitation.volume","305"],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Biermann, Daniel"],["dc.contributor.author","Buchert, Ralph"],["dc.contributor.author","Hess, Andreas"],["dc.contributor.author","Wittkoepper, Katrin"],["dc.contributor.author","Christalla, Peter"],["dc.contributor.author","Doeker, Stephan"],["dc.contributor.author","Jebran, Fawad"],["dc.contributor.author","Schoendube, Friedrich"],["dc.contributor.author","Reichenspurner, Hermann"],["dc.contributor.author","El-Armouche, Ali"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.date.accessioned","2017-09-07T11:47:38Z"],["dc.date.available","2017-09-07T11:47:38Z"],["dc.date.issued","2013"],["dc.description.abstract","Total mechanical unloading of the heart in classical models of heterotopic heart transplantation leads to cardiac atrophy and functional deterioration. In contrast, partial unloading of failing human hearts with left ventricular (LV) assist devices (LVADs) can in some patients ameliorate heart failure symptoms. Here we tested in heterotopic rat heart transplant models whether partial volume-loading (VL; anastomoses: aorta of donor to aorta of recipient, pulmonary artery of donor to left atrium of donor, superior vena cava of donor to inferior vena cava of recipient; n = 27) is superior to the classical model of myocardial unloading (UL; anastomoses: aorta of donor to aorta of recipient, pulmonary artery of donor to inferior vena cava of recipient; n = 14) with respect to preservation of ventricular morphology and function. Echocardiography, magnetic resonance imaging, and LV-pressure-volume catheter revealed attenuated myocardial atrophy with similar to 30% higher LV weight and better systolic contractile function in VL compared with UL (fractional area shortening, 34% vs. 18%; maximal change in pressure over time, 2,986 +/- 252 vs. 2,032 +/- 193 mmHg/s). Interestingly, no differences in fibrosis (Picrosirus red staining) or glucose metabolism (2-[18F]-fluoro-2-deoxy-D-glucose-PET) between VL and UL were observed. We conclude that the rat model of partial VL attenuates atrophic remodelling and shows superior morphological as well as functional preservation, and thus should be considered more widely as a research model."],["dc.identifier.doi","10.1152/ajpheart.00218.2013"],["dc.identifier.gro","3142311"],["dc.identifier.isi","000323549500009"],["dc.identifier.pmid","23771692"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/6875"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/11"],["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.issn","0363-6135"],["dc.relation.workinggroup","RG El-Armouche"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.title","Preservation of left ventricular function and morphology in volume-loaded versus volume-unloaded heterotopic heart transplants"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","21"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.volume","124"],["dc.contributor.author","Neef, Stefan"],["dc.contributor.author","Wittkoepper, Katrin"],["dc.contributor.author","Brammen, Christina"],["dc.contributor.author","Sowa, Thomas"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Brown, Joan Heller"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","El-Armouche, Ali"],["dc.date.accessioned","2018-11-07T08:49:43Z"],["dc.date.available","2018-11-07T08:49:43Z"],["dc.date.issued","2011"],["dc.identifier.isi","000299738707260"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21531"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.issn","0009-7322"],["dc.title","Ablation of Phosphatase-1-Inhibitor-1 is Detrimental in CaMKII Overexpression Despite Reduction of SR Ca2+Leak"],["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","383"],["dc.contributor.author","Wittkoepper, Katrin"],["dc.contributor.author","Emons, J."],["dc.contributor.author","Mehel, Hind"],["dc.contributor.author","Sossalla, Samuel T."],["dc.contributor.author","Vandecasteele, Gregoire"],["dc.contributor.author","Fischmeister, Rodolphe"],["dc.contributor.author","El-Armouche, Ali"],["dc.date.accessioned","2018-11-07T08:58:32Z"],["dc.date.available","2018-11-07T08:58:32Z"],["dc.date.issued","2011"],["dc.format.extent","60"],["dc.identifier.isi","000288573100299"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23665"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.conference","77th Annual Meeting on German-Society-for-Experimental-and-Clinical-Pharmacology-and-Toxicology"],["dc.relation.eventlocation","Frankfurt, GERMANY"],["dc.relation.issn","0028-1298"],["dc.title","Evidence for Phosphodiesterase 2A playing a role in human and experimental heart failure"],["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","383"],["dc.contributor.author","Ewens, S."],["dc.contributor.author","Wittkoepper, Katrin"],["dc.contributor.author","Emons, J."],["dc.contributor.author","Laemmle, Simon"],["dc.contributor.author","Lutz, S."],["dc.contributor.author","El-Armouche, Ali"],["dc.date.accessioned","2018-11-07T08:58:34Z"],["dc.date.available","2018-11-07T08:58:34Z"],["dc.date.issued","2011"],["dc.format.extent","68"],["dc.identifier.isi","000288573100340"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23673"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.eventlocation","Frankfurt, GERMANY"],["dc.relation.issn","0028-1298"],["dc.title","Phosphatase-inhibitor-1 activation is mediated via beta(2)-adrenoceptors in cardiac fibroblasts"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Circulation Research"],["dc.bibliographiccitation.volume","103"],["dc.contributor.author","Wittkoepper, Katrin"],["dc.contributor.author","Fabritz, Larissa"],["dc.contributor.author","Kirchhof, Paulus"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Geertz, Birgit"],["dc.contributor.author","Dobrev, Dobromir"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.contributor.author","El-Armouche, Ali"],["dc.date.accessioned","2018-11-07T11:08:12Z"],["dc.date.available","2018-11-07T11:08:12Z"],["dc.date.issued","2008"],["dc.format.extent","1497"],["dc.identifier.isi","000261418900033"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52721"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","81st Annual Scientific Session of the American-Heart-Association"],["dc.relation.eventlocation","New Orleans, LA"],["dc.relation.issn","0009-7330"],["dc.title","Phosphatase-1-Inhibitor-1 Improves Contractile Performance but Increases Propensity toward Arrhythmias and Contractile Dysfunction after Pathological beta-adrenergic Stimulation in Mice"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","340"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Biochemical and Biophysical Research Communications"],["dc.bibliographiccitation.lastpage","344"],["dc.bibliographiccitation.volume","402"],["dc.contributor.author","El-Armouche, Ali"],["dc.contributor.author","Wahab, Azadeh"],["dc.contributor.author","Wittkoepper, Katrin"],["dc.contributor.author","Schulze, Thomas"],["dc.contributor.author","Boettcher, Felix"],["dc.contributor.author","Pohlmann, Lutz"],["dc.contributor.author","King, S. Bruce"],["dc.contributor.author","DuMond, Jenna F."],["dc.contributor.author","Gerloff, Christian"],["dc.contributor.author","Boeger, Rainer H."],["dc.contributor.author","Eschenhagen, Thomas"],["dc.contributor.author","Carrier, Lucie"],["dc.contributor.author","Donzelli, Sonia"],["dc.date.accessioned","2018-11-07T08:36:57Z"],["dc.date.available","2018-11-07T08:36:57Z"],["dc.date.issued","2010"],["dc.description.abstract","Contractile dysfunction and diminished response to p-adrenergic agonists are characteristics for failing hearts. Chemically donated nitroxyl (HNO) improves contractility in failing hearts and thus may have therapeutic potential. Yet, there is a need for pharmacologically suitable donors. In this study we tested whether the pure and long acting HNO donor, 1-nitrosocyclohexyl acetate (NCA), affects contractile force in normal and pathological ventricular myocytes (VMs) as well as in isolated hearts. VMs were isolated from mice either subjected to isoprenaline-infusion (ISO; 30 mu g/g per day) or to vehicle (0.9% NaCl) for 5 days. Sarcomere shortening and Ca(2+) transients were simultaneously measured using the IonOptix system. Force of contraction of isolated hearts was measured by a Langendorff-perfusion system. NCA increased peak sarcomere shortening by + 40-200% in a concentration-dependent manner (EC(50) similar to 55 mu M). Efficacy and potency did not differ between normal and chronic ISO VMs, despite the fact that the latter displayed a markedly diminished inotropic response to acute p-adrenergic stimulation with ISO (1 mu M). NCA (60 mu M) increased peak sarcomere shortening and Ca(2+) transient amplitude by similar to 200% and similar to 120%, respectively, suggesting effects on both myofilament Ca2+ sensitivity and sarcoplasmic reticulum (SR) Ca(2+) cycling. Importantly, NCA did not affect diastolic Ca(2+) or SR Ca(2+) content, as assessed by rapid caffeine application. NCA (45 mu M) increased force of contraction by 30% in isolated hearts. In conclusion, NCA increased contractile force in normal and beta-adrenergically desensitized VMs as well as in isolated mouse hearts. This profile warrants further investigations of this HNO donor in the context of heart failure. (C) 2010 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.bbrc.2010.10.030"],["dc.identifier.isi","000284862300032"],["dc.identifier.pmid","20946877"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18424"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Inc Elsevier Science"],["dc.relation.issn","0006-291X"],["dc.title","The new HNO donor, 1-nitrosocyclohexyl acetate, increases contractile force in normal and beta-adrenergically desensitized ventricular myocytes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","4467"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","The FASEB Journal"],["dc.bibliographiccitation.lastpage","4475"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","El-Armouche, Ali"],["dc.contributor.author","Wittkoepper, Katrin"],["dc.contributor.author","Fuller, William"],["dc.contributor.author","Howie, Jacqueline"],["dc.contributor.author","Shattock, Michael J."],["dc.contributor.author","Pavlovic, Davor"],["dc.date.accessioned","2018-11-07T08:49:09Z"],["dc.date.available","2018-11-07T08:49:09Z"],["dc.date.issued","2011"],["dc.description.abstract","Cardiac Na/K-ATPase (NKA) is regulated by its accessory protein phospholemman (PLM). Whereas kinase-induced PLM phosphorylation has been shown to mediate NKA stimulation, the role of endogenous phosphatases is presently unknown. We investigated the role of protein phosphatase-1 (PP-1) on PLM phosphorylation and NKA activity in rat cardiomyocytes and failing human hearts. Incubation of rat cardiomyocytes with the chemical PP-1/PP-2A inhibitor okadaic acid or the specific PP-1-inhibitor peptide (I-1ct) identified PLM phosphorylation at Ser-68 as the main substrate for PP-1. Moreover, myocytes adenovirally overexpressing PP-1 inhibitor-1 protein (I-1,Ad-I-1/eGFP) showed a 70% increase in PLM Ser-68 phosphorylation and 65% increase in NKA current, compared with enhanced green fluorescence protein (eGFP)-infected controls (Ad-eGFP), using Western blotting and voltage clamping, respectively. Notably, in left ventricular myocardium from patients with heart failure, PLM Ser-68 phosphorylation was similar to 50% lower (n=7) than in nonfailing controls (n=7). We provide the first physiological and biochemical evidence that PLM phosphorylation and cardiac Na/K-ATPase activity are negatively regulated by PP-1 and that this regulatory mechanism could be counteracted by I-1. This novel mechanism is markedly perturbed in failing hearts favoring PLM dephosphorylation and NKA deactivation and thus may contribute to maladaptive hypertrophy and arrhythmogenesis via chronically higher intracellular Na and Ca concentrations.-El-Armouche, A., Wittkopper, K., Fuller, W., Howie, J., Shattock, M. J., Pavlovic, D. Phospholemman-dependent regulation of the cardiac Na/K-ATPase activity is modulated by inhibitor-1 sensitive type-1 phosphatase. FASEB J. 25, 4467-4475 (2011). www.fasebj.org"],["dc.identifier.doi","10.1096/fj.11-184903"],["dc.identifier.isi","000298138100037"],["dc.identifier.pmid","21849407"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21389"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Federation Amer Soc Exp Biol"],["dc.relation.issn","0892-6638"],["dc.title","Phospholemman-dependent regulation of the cardiac Na/K-ATPase activity is modulated by inhibitor-1 sensitive type-1 phosphatase"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","371"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Molecular and Cellular Cardiology"],["dc.bibliographiccitation.lastpage","376"],["dc.bibliographiccitation.volume","43"],["dc.contributor.author","El-Armouche, Ali"],["dc.contributor.author","Singh, Jasmin"],["dc.contributor.author","Naito, Hiroshi"],["dc.contributor.author","Wittkoepper, Katrin"],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Laatsch, Alexander"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.date.accessioned","2017-09-07T11:49:25Z"],["dc.date.available","2017-09-07T11:49:25Z"],["dc.date.issued","2007"],["dc.description.abstract","PKC alpha has been shown to be a negative regulator of contractility and PKCa gene deletion in mice protected against heart failure. Small interfering (si)RNAs mediate gene silencing by RNA interference (RNAi) and may be used to knockdown PKC alpha in cardiomyocytes. However, transfection efficiencies of (si)RNAs by lipofection tend to be low in primary cells. To address this limitation, we developed an adenoviral vector (AV) driving short hairpin (sh)RNAs against PKCa (Ad-shPKC alpha) and evaluated its potential to silence PKCa in neonatal rat cardiac myocytes and in engineered heart tissues (EHTs), which resemble functional myocardium in vitro. A nonsense encoding AV (Ad-shNS) served as control. Quantitative PCR and Western blotting showed 90% lower PKC alpha.-mRNA and 50% lower PKC alpha protein in Ad-shPKC alpha-infected cells. EHTs were infected with Ad-shPKCa on day I I and subjected to isometric force measurements in organ baths 4 days later. Mean twitch tension was > 50% higher in Ad-shPKC alpha compared to Ad-shNS-infected EHTs, under basal and Ca2+- or isoprenaline-stimulated conditions. Twitch tension negatively correlated with PKCa mRNA levels. In summary, AV-delivered shRNA mediated highly efficient PKCa knockdown in cardiac myocytes and improved contractility in EHTs. The data support a role of PKC alpha as a negative regulator of myocardial contractility and demonstrate that EHTs in conjunction with AV-delivered shRNA are a useful model for target validation. (c) 2007 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.yjmcc.2007.05.021"],["dc.identifier.gro","3143445"],["dc.identifier.isi","000249611300016"],["dc.identifier.pmid","17628588"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/960"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Academic Press Ltd- Elsevier Science Ltd"],["dc.relation.eissn","1095-8584"],["dc.relation.issn","0022-2828"],["dc.title","Adenovirus-delivered short hairpin RNA targeting contractile function in reconstituted heart PKC alpha improves tissue"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","European Journal of Heart Failure"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Vettel, Christiane"],["dc.contributor.author","Laemmle, Simon"],["dc.contributor.author","Emons, J."],["dc.contributor.author","Ewens, S."],["dc.contributor.author","Cervirgen, C."],["dc.contributor.author","Wittkoepper, Katrin"],["dc.contributor.author","Wuertz, Christina M."],["dc.contributor.author","Lutz, S."],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","El-Armouche, Ali"],["dc.date.accessioned","2018-11-07T09:25:44Z"],["dc.date.available","2018-11-07T09:25:44Z"],["dc.date.issued","2013"],["dc.format.extent","S64"],["dc.identifier.isi","000332489100238"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30137"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.issn","1879-0844"],["dc.relation.issn","1388-9842"],["dc.title","Phosphodiesterase 2 activates myofibroblast formation and CTGF synthesis in cardiac fibroblasts and augments stiffness in engineered connective tissue"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]