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001-es BibID:BIBFORM015074
Első szerző:Borbély Attila (kardiológus)
Cím:Cardiomyocyte Stiffness in Diastolic Heart Failure / Borbély A., van der Velden J., Papp Z., Bronzwaer J. G. F., Edes I., Stienen G. J. M., Paulus W. J.
Dátum:2005
ISSN:0009-7322
Megjegyzések:Heart failure with preserved left ventricular (LV) ejection fraction (EF) is increasingly recognized and usually referred to as diastolic heart failure (DHF). Its pathogenetic mechanism remains unclear, partly because of a lack of myocardial biopsy material. Endomyocardial biopsy samples obtained from DHF patients were therefore analyzed for collagen volume fraction (CVF) and sarcomeric protein composition and compared with control samples. Single cardiomyocytes were isolated from these biopsy samples to assess cellular contractile performance.METHODS AND RESULTS: DHF patients (n=12) had an LVEF of 71+/-11%, an LV end-diastolic pressure (LVEDP) of 28+/-4 mm Hg, and no significant coronary artery stenoses. DHF patients had higher CVFs (7.5+/-4.0%, P<0.05) than did controls (n=8, 3.8+/-2.0%), and no conspicuous changes in sarcomeric protein composition were detected. Cardiomyocytes, mechanically isolated and treated with Triton X-100 to remove all membranes, were stretched to a sarcomere length of 2.2 microm and activated with solutions containing varying [Ca2+]. Compared with cardiomyocytes of controls, cardiomyocytes of DHF patients developed a similar total isometric force at maximal [Ca2+], but their resting tension (F(passive)) in the absence of Ca2+ was almost twice as high (6.6+/-3.0 versus 3.5+/-1.7 kN/m2, P<0.001). F(passive) and CVF combined yielded stronger correlations with LVEDP than did either alone. Administration of protein kinase A (PKA) to DHF cardiomyocytes lowered F(passive) to control values.CONCLUSIONS: DHF patients had stiffer cardiomyocytes, as evident from a higher F(passive) at the same sarcomere length. Together with CVF, F(passive) determined in vivo diastolic LV dysfunction. Correction of this high F(passive) by PKA suggests that reduced phosphorylation of sarcomeric proteins is involved in DHF.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Circulation. - 111 : 6 (2005), p. 774-781. -
További szerzők:Velden, Jolanda, van der Papp Zoltán (1965-) (kardiológus, élettanász) Bronzwaer, Jean G. F. Édes István (1952-) (kardiológus) Stienen, Ger J. M. Paulus, Walter J.
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2.

001-es BibID:BIBFORM010415
Első szerző:Borbély Attila (kardiológus)
Cím:Hypophosphorylation of the Stiff N2B titin isoform raises cardiomyocyte resting tension in failing human myocardium / Borbely, A., Falcao-Pires, I., van Heerebeek, L., Hamdani, N., Edes, I., Gavina, C., Leite-Moreira, A. F., Bronzwaer, J. G. F., Papp, Z., van der Velden, J., Stienen, G. J. M., Paulus, W. J.
Dátum:2009
ISSN:1524-4571 (Electronic)
Megjegyzések:High diastolic stiffness of failing myocardium results from interstitial fibrosis and elevated resting tension (F(passive)) of cardiomyocytes. A shift in titin isoform expression from N2BA to N2B isoform, lower overall phosphorylation of titin, and a shift in titin phosphorylation from N2B to N2BA isoform can raise F(passive) of cardiomyocytes. In left ventricular biopsies of heart failure (HF) patients, aortic stenosis (AS) patients, and controls (CON), we therefore related F(passive) of isolated cardiomyocytes to expression of titin isoforms and to phosphorylation of titin and titin isoforms. Biopsies were procured by transvascular technique (44 HF, 3 CON), perioperatively (25 AS, 4 CON), or from explanted hearts (4 HF, 8 CON). None had coronary artery disease. Isolated, permeabilized cardiomyocytes were stretched to 2.2-microm sarcomere length to measure F(passive). Expression and phosphorylation of titin isoforms were analyzed using gel electrophoresis with ProQ Diamond and SYPRO Ruby stains and reported as ratio of titin (N2BA/N2B) or of phosphorylated titin (P-N2BA/P-N2B) isoforms. F(passive) was higher in HF (6.1+/-0.4 kN/m(2)) than in CON (2.3+/-0.3 kN/m(2); P<0.01) or in AS (2.2+/-0.2 kN/m(2); P<0.001). Titin isoform expression differed between HF (N2BA/N2B=0.73+/-0.06) and CON (N2BA/N2B=0.39+/-0.05; P<0.001) and was comparable in HF and AS (N2BA/N2B=0.59+/-0.06). Overall titin phosphorylation was also comparable in HF and AS, but relative phosphorylation of the stiff N2B titin isoform was significantly lower in HF (P-N2BA/P-N2B=0.77+/-0.05) than in AS (P-N2BA/P-N2B=0.54+/-0.05; P<0.01). Relative hypophosphorylation of the stiff N2B titin isoform is a novel mechanism responsible for raised F(passive) of human HF cardiomyocytes.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Aged
Biopsy
Elasticity
Female
Heart Failure
Humans
Male
Middle Aged
Muscle Proteins
Myocardium
Myocytes, Cardiac
Phosphorylation
Protein Isoforms
Protein Kinases
Sarcomeres
Megjelenés:Circulation Research. - 104 : 6 (2009), p. 780-786. -
További szerzők:Falcao-Pires, Ines Heerebeek, Loek, van Hamdani, Nazha Édes István (1952-) (kardiológus) Gavina, Cristina Leite-Moreira, Adelino F. Bronzwaer, Jean G. F. Papp Zoltán (1965-) (kardiológus, élettanász) Velden, Jolanda, van der Stienen, Ger J. M. Paulus, Walter J.
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3.

001-es BibID:BIBFORM010421
Első szerző:Hamdani, Nazha
Cím:Distinct myocardial effects of beta-blocker therapy in heart failure with normal and reduced left ventricular ejection fraction / Hamdani, N., Paulus, W. J., van Heerebeek, L., Borbely, A., Boontje, N. M., Zuidwijk, M. J., Bronzwaer, J. G., Simonides, W. S., Niessen, H. W., Stienen, G. J. M., van der Velden, J.
Dátum:2009
ISSN:0195-668X (Print)
Megjegyzések:Left ventricular (LV) myocardial structure and function differ in heart failure (HF) with normal (N) and reduced (R) LV ejection fraction (EF). This difference could underlie an unequal outcome of trials with beta-blockers in heart failure with normal LVEF (HFNEF) and heart failure with reduced LVEF (HFREF) with mixed results observed in HFNEF and positive results in HFREF. To investigate whether beta-blockers have distinct myocardial effects in HFNEF and HFREF, myocardial structure, cardiomyocyte function, and myocardial protein composition were compared in HFNEF and HFREF patients without or with beta-blockers. METHODS AND RESULTS: Patients, free of coronary artery disease, were divided into beta-(HFNEF) (n = 16), beta+(HFNEF) (n = 16), beta-(HFREF) (n = 17), and beta+(HFREF) (n = 22) groups. Using LV endomyocardial biopsies, we assessed collagen volume fraction (CVF) and cardiomyocyte diameter (MyD) by histomorphometry, phosphorylation of myofilamentary proteins by ProQ-Diamond phosphostained 1D-gels, and expression of beta-adrenergic signalling and calcium handling proteins by western immunoblotting. Cardiomyocytes were also isolated from the biopsies to measure active force (F(active)), resting force (F(passive)), and calcium sensitivity (pCa(50)). Myocardial effects of beta-blocker therapy were either shared by HFNEF and HFREF, unique to HFNEF or unique to HFREF. Higher F(active), higher pCa(50), lower phosphorylation of troponin I and myosin-binding protein C, and lower beta(2) adrenergic receptor expression were shared. Higher F(passive), lower CVF, lower MyD, and lower expression of stimulatory G protein were unique to HFNEF and lower expression of inhibitory G protein was unique to HFREF. CONCLUSION: Myocardial effects unique to either HFNEF or HFREF could contribute to the dissimilar outcome of beta-blocker therapy in both HF phenotypes.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Adrenergic beta-Antagonists
Aged
Cross-Sectional Studies
Female
Heart Failure
Humans
Male
Microfilament Proteins
Middle Aged
Myocardium
Myocytes, Cardiac
Phosphorylation
Stroke Volume
Ventricular Dysfunction, Left
Megjelenés:European Heart Journal. - 30 : 15 (2009), p. 1863-1872. -
További szerzők:Paulus, Walter J. Heerebeek, Loek, van Borbély Attila (1978-) (kardiológus) Boontje, Nicky M. Zuidwijk, Marian J. Bronzwaer, Jean G. F. Simonides, Warner S. Niessen, Hans W. M. Stienen, Ger J. M. Velden, Jolanda, van der
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM030333
Első szerző:Heerebeek, Loek, van
Cím:Response to Letter Regarding Article, "Diastolic Stiffness of the Failing Diabetic Heart : Importance of Fibrosis, Advanced Glycation End Products, and Myocyte Resting Tension" / van Heerebeek L., Hamdani N., Handoko M. L., Falcao-Pires I., Musters R. J., Kupreishvili K., Ijsselmuiden A. J., Schalkwijk C. G., Bronzwaer J. G., Diamant M., Borbely A., van der Velden J., Stienen G. J. M., Laarman G. J., Niessen H. W., Paulus W. J.
Dátum:2008
ISSN:0009-7322
Tárgyszavak:Orvostudományok Elméleti orvostudományok levél
Megjelenés:Circulation. - 117 (2008), p. e484. -
További szerzők:Hamdani, Nazha Handoko, Martin Louis Falcao-Pires, Ines Musters, René J. Kupreishvili, Koba Ijsselmuiden, Alexander J. J. Schalkwijk, Casper G. Bronzwaer, Jean G. F. Diamant, Michaela Borbély Attila (1978-) (kardiológus) Velden, Jolanda, van der Stienen, Ger J. M. Laarman, Gerrit J. Niessen, Hans W. M. Paulus, Walter J.
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5.

001-es BibID:BIBFORM014721
Első szerző:Heerebeek, Loek, van
Cím:Myocardial Structure and Function Differ in Systolic and Diastolic Heart Failure / van Heerebeek L., Borbély A., Niessen H. W. M., Bronzwaer J. G. F., van der Velden J., Stienen G. J., Linke W. A., Laarman G. J., Paulus W. J.
Dátum:2006
ISSN:0009-7322
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Circulation. - 113 : 16 (2006), p. 1966-1973. -
További szerzők:Borbély Attila (1978-) (kardiológus) Niessen, Hans W. M. Bronzwaer, Jean G. F. Velden, Jolanda, van der Stienen, Ger J. M. Linke, Wolfgang A. Laarman, Gerrit J. Paulus, Walter J.
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6.

001-es BibID:BIBFORM005642
Első szerző:Heerebeek, Loek, van
Cím:Diastolic stiffness of the failing diabetic heart : importance of fibrosis, advanced glycation end products, and myocyte resting tension / van Heerebeek, L., Hamdani, N., Handoko, M. L., Falcao-Pires, I., Musters, R. J., Kupreishvili, K., Ijsselmuiden, A. J. J., Schalkwijk, C. G., Bronzwaer, J. G. F., Diamant, M., Borbely, A., van der Velden, J., Stienen, G. J. M., Laarman, G. J., Niessen, H. W. M., Paulus, W. J.
Dátum:2008
ISSN:1524-4539 (Electronic)
Megjegyzések:Excessive diastolic left ventricular stiffness is an important contributor to heart failure in patients with diabetes mellitus. Diabetes is presumed to increase stiffness through myocardial deposition of collagen and advanced glycation end products (AGEs). Cardiomyocyte resting tension also elevates stiffness, especially in heart failure with normal left ventricular ejection fraction (LVEF). The contribution to diastolic stiffness of fibrosis, AGEs, and cardiomyocyte resting tension was assessed in diabetic heart failure patients with normal or reduced LVEF. METHODS AND RESULTS: Left ventricular endomyocardial biopsy samples were procured in 28 patients with normal LVEF and 36 patients with reduced LVEF, all without coronary artery disease. Sixteen patients with normal LVEF and 10 with reduced LVEF had diabetes mellitus. Biopsy samples were used for quantification of collagen and AGEs and for isolation of cardiomyocytes to measure resting tension. Diabetic heart failure patients had higher diastolic left ventricular stiffness irrespective of LVEF. Diabetes mellitus increased the myocardial collagen volume fraction only in patients with reduced LVEF (from 14.6+/-1.0% to 22.4+/-2.2%, P<0.001) and increased cardiomyocyte resting tension only in patients with normal LVEF (from 5.1+/-0.7 to 8.5+/-0.9 kN/m2, P=0.006). Diabetes increased myocardial AGE deposition in patients with reduced LVEF (from 8.8+/-2.5 to 24.1+/-3.8 score/mm2; P=0.005) and less so in patients with normal LVEF (from 8.2+/-2.5 to 15.7+/-2.7 score/mm2, P=NS). CONCLUSIONS: Mechanisms responsible for the increased diastolic stiffness of the diabetic heart differ in heart failure with reduced and normal LVEF: Fibrosis and AGEs are more important when LVEF is reduced, whereas cardiomyocyte resting tension is more important when LVEF is normal.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Case-Control Studies
Diabetes Complications/ physiopathology
Diabetes Mellitus/physiopathology
Diastole
Female
Fibrosis
Glycosylation End Products, Advanced
Heart Failure/etiology/ pathology
Heart Ventricles/pathology
Humans
Male
Middle Aged
Muscle Tonus
Myocytes, Cardiac/ physiology
Stroke Volume
Megjelenés:Circulation. - 117 : 1 (2008), p. 43-51. -
További szerzők:Hamdani, Nazha Handoko, Martin Louis Falcao-Pires, Ines Musters, René J. Kupreishvili, Koba Ijsselmuiden, Alexander J. J. Schalkwijk, Casper G. Bronzwaer, Jean G. F. Diamant, Michaela Borbély Attila (1978-) (kardiológus) Velden, Jolanda, van der Stienen, Ger J. M. Laarman, Gerrit J. Niessen, Hans W. M. Paulus, Walter J.
Internet cím:elektronikus változat
DOI
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7.

001-es BibID:BIBFORM015092
Első szerző:Velden, Jolanda, van der
Cím:Functional effects of protein kinase C-mediated myofilament phosphorylation in human myocardium / van der Velden J., Narolska N. A., Lamberts R. R., Boontje N. M., Borbély A., Zaremba R., Bronzwaer J. G. F., Papp Z., Jaquet K., Paulus W. J., Stienen G. J.
Dátum:2006
ISSN:0008-6363
Megjegyzések:In human heart failure beta-adrenergic-mediated protein kinase A (PKA) activity is down-regulated, while protein kinase C (PKC) activity is up-regulated. PKC-mediated myofilament protein phosphorylation might be detrimental for contractile function in cardiomyopathy. This study was designed to reveal the effects of PKC on myofilament function in human myocardium under basal conditions and upon modulation of protein phosphorylation by PKA and phosphatases.METHODS: Isometric force was measured at different [Ca(2+)] in single permeabilized cardiomyocytes from non-failing and failing human left ventricular tissue. Basal phosphorylation of myofilament proteins and the influence of PKC, PKA, and phosphatase treatments were analyzed by one- and two-dimensional gel electrophoresis, Western immunoblotting, and ELISA.RESULTS: Troponin I (TnI) phosphorylation at the PKA sites was decreased in failing compared to non-failing hearts and correlated well with myofilament Ca(2+) sensitivity (pCa(50)). Incubation with the catalytic domain of PKC slightly decreased maximal force under basal conditions, but not following PKA and phosphatase pretreatments. PKC reduced Ca(2+) sensitivity to a larger extent in failing (DeltapCa(50)=0.19+/-0.03) than in non-failing (DeltapCa(50)=0.08+/-0.01) cardiomyocytes. This shift was reduced, though still significant, when PKC was preceded by PKA, while PKA following PKC did not further decrease pCa(50). Protein analysis indicated that PKC phosphorylated PKA sites in human TnI and increased phosphorylation of troponin T, while myosin light chain phosphorylation remained unaltered.CONCLUSION: In human myocardium PKC-mediated myofilament protein phosphorylation only has a minor effect on maximal force development. The PKC-mediated decrease in Ca(2+) sensitivity may serve to improve diastolic function in failing human myocardium in which PKA-mediated TnI phosphorylation is decreased.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Cardiovascular Research. - 69 : 4 (2006), p. 876-887. -
További szerzők:Narolska, Nadiya A. Lamberts, Regis Boontje, Nicky M. Borbély Attila (1978-) (kardiológus) Zaremba, Ruud Bronzwaer, Jean G. F. Papp Zoltán (1965-) (kardiológus, élettanász) Jaquet, Kornelia Paulus, Walter J. Stienen, Ger J. M.
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