El-Armouche, Ali

[["dc.bibliographiccitation.firstpage","1150"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Circulation Research"],["dc.bibliographiccitation.lastpage","U215"],["dc.bibliographiccitation.volume","107"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Fluschnik, Nina"],["dc.contributor.author","Schotola, Hanna"],["dc.contributor.author","Ort, Katharina R."],["dc.contributor.author","Neef, Stefan"],["dc.contributor.author","Schulte, Timo"],["dc.contributor.author","Wittkoepper, Katrin"],["dc.contributor.author","Renner, André"],["dc.contributor.author","Schmitto, Jan D."],["dc.contributor.author","Gummert, Jan"],["dc.contributor.author","El-Armouche, Ali"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Maier, Lars S."],["dc.date.accessioned","2017-09-07T11:45:15Z"],["dc.date.available","2017-09-07T11:45:15Z"],["dc.date.issued","2010"],["dc.description.abstract","Rationale: Heart failure (HF) is known to be associated with increased Ca2+/calmodulin-dependent protein kinase (CaMK)II expression and activity. There is still controversial discussion about the functional role of CaMKII in HF. Moreover, CaMKII inhibition has never been investigated in human myocardium. Objective: We sought to investigate detailed CaMKII delta expression in end-stage failing human hearts (dilated and ischemic cardiomyopathy) and the functional effects of CaMKII inhibition on contractility. Methods and Results: Expression analysis revealed that CaMKII delta, both cytosolic delta(C) and nuclear delta(B) splice variants, were significantly increased in both right and left ventricles from patients with dilated or ischemic cardiomyopathy versus nonfailing. Experiments with isometrically twitching trabeculae revealed significantly improved force frequency relationships in the presence of CaMKII inhibitors (KN-93 and AIP). Increased postrest twitches after CaMKII inhibition indicated an improved sarcoplasmic reticulum (SR) Ca2+ loading. This was confirmed in isolated myocytes by a reduced SR Ca2+ spark frequency and hence SR Ca2+ leak, resulting in increased SR Ca2+ load when inhibiting CaMKII. Ryanodine receptor type 2 phosphorylation at Ser2815, which is known to be phosphorylated by CaMKII thereby contributing to SR Ca2+ leak, was found to be markedly reduced in KN-93-treated trabeculae. Interestingly, CaMKII inhibition did not influence contractility in nonfailing sheep trabeculae. Conclusions: The present study shows for the first time that CaMKII inhibition acutely improves contractility in human HF where CaMKII delta expression is increased. The mechanism proposed consists of a reduced SR Ca2+ leak and consequently increased SR Ca2+ load. Thus, CaMKII inhibition appears to be a possible therapeutic option for patients with HF and merits further investigation. (Circ Res. 2010;107:1150-1161.)"],["dc.identifier.doi","10.1161/CIRCRESAHA.110.220418"],["dc.identifier.gro","3142840"],["dc.identifier.isi","000283583400015"],["dc.identifier.pmid","20814023"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6154"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/288"],["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.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0009-7330"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Inhibition of Elevated Ca2+/Calmodulin-Dependent Protein Kinase II Improves Contractility in Human Failing Myocardium"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","621"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Circulation Heart Failure"],["dc.bibliographiccitation.lastpage","627"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","El-Armouche, Ali"],["dc.contributor.author","Ouchi, Noriyuki"],["dc.contributor.author","Tanaka, Komei"],["dc.contributor.author","Doros, Gheorghe"],["dc.contributor.author","Wittkoepper, Katrin"],["dc.contributor.author","Schulze, Thomas"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.contributor.author","Walsh, Kenneth"],["dc.contributor.author","Sam, Flora"],["dc.date.accessioned","2018-11-07T08:52:26Z"],["dc.date.available","2018-11-07T08:52:26Z"],["dc.date.issued","2011"],["dc.description.abstract","Background-Follistatin-like 1 (FSTL1) is an extracellular glycoprotein found in human serum. Recent work suggests that FSTL1 is secreted in response to ischemic injuries and that its overexpression is protective in the heart and vasculature. Methods and Results-We examined serum FSTL1 levels in patients with chronic heart failure with left ventricular (LV) ejection fraction <40% (n=86). The sample was separated into three tertiles of patients with low, medium, and high FSTL1 levels. Serum FSTL1 was increased 56% above age-and sex-matched healthy controls. Diabetes mellitus, brain natriuretic peptide level, left atrial size, LV posterior wall thickness, LV end-diastolic diameter, and LV mass were significant determinants of FSTL1 serum levels by bivariate analysis. After controlling for significant covariates, FSTL1 levels predicted LV hypertrophy (as measured by LV mass index) by multivariate linear regression analysis (P<0.001). Unadjusted survival analysis demonstrated increased mortality in patients with increasing FSTL1 levels (P=0.09). After adjusting for significant parameters, patients with increased FSTL1 remained at the highest risk of death (hazard ratio, 1.028; 95% CI, 0.98 to 1.78; P=0.26). To determine whether elevated FSTL1 levels may be derived from the myocardium, FSTL1 protein expression was measured in explanted failing (n=18) and nonfailing (n=7) human hearts. LV failing hearts showed 2.5-fold higher FSTL1 protein levels over nonfailing control hearts (P<.05). Conclusions-Elevated serum FSTL1 in patients with heart failure was associated with LV hypertrophy. Further studies on the role of FSTL1 as a biomarker in chronic systolic heart failure are warranted. (Circ Heart Fail. 2011;4:621-627.)"],["dc.description.sponsorship","National Heart, Lung, and Blood Institute [HL102631, HL079099]"],["dc.identifier.doi","10.1161/CIRCHEARTFAILURE.110.960625"],["dc.identifier.isi","000295035000015"],["dc.identifier.pmid","21622850"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8227"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22163"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","1941-3289"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Follistatin-Like 1 in Chronic Systolic Heart Failure A Marker of Left Ventricular Remodeling"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["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","569"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Basic Research in Cardiology"],["dc.bibliographiccitation.lastpage","571"],["dc.bibliographiccitation.volume","105"],["dc.contributor.author","Wittkoepper, Katrin"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.contributor.author","El-Armouche, Ali"],["dc.date.accessioned","2018-11-07T08:39:30Z"],["dc.date.available","2018-11-07T08:39:30Z"],["dc.date.issued","2010"],["dc.identifier.doi","10.1007/s00395-010-0107-2"],["dc.identifier.isi","000280647500001"],["dc.identifier.pmid","20526608"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/4984"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19012"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","0300-8428"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Phosphatase-1-inhibitor-1: amplifier or attenuator of catecholaminergic stress?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dc.type.version","published_version"],["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"]]