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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:BIBFORM003575
Első szerző:Borbély Attila (kardiológus)
Cím:Peroxynitrite-induced alpha-actinin nitration and contractile alterations in isolated human myocardial cells / Borbély A., Tóth A., Édes I., Virág L., Papp J. G., Varró A., Paulus W. J., van der Velden J., Stienen G. J. M., Papp Z.
Dátum:2005
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
myocytes
contractile function
peroxynitrite
alpha-actinin
human myocardium
Megjelenés:Cardiovascular Research. - 67 : 2 (2005), p. 225-233. -
További szerzők:Tóth Attila (1971-) (biológus) Édes István (1952-) (kardiológus) Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Papp Gy. Julius (Szeged) Varró András (1954-) (farmakológus, klinikai farmakológus) Paulus, Walter J. Velden, Jolanda, van der Stienen, Ger J. M. Papp Zoltán (1965-) (kardiológus, élettanász)
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4.

001-es BibID:BIBFORM002144
Első szerző:Édes István Ferenc (kardiológus)
Cím:Rate of tension redevelopment is not modulated by sarcomere length in permeabilized human, murine, and porcine cardiomyocytes / Edes I. F., Czuriga D., Csányi G., Chlopicki S., Recchia F. A., Borbély A., Galajda Z., Edes I., van der Velden J., Stienen G. J., Papp Z.
Dátum:2007
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:American Journal of Physiology. Regulatory, Integrative and Comparative Physiology. - 293 : 1 (2007), p. R20-R29. -
További szerzők:Czuriga Dániel (1982-) (kardiológus) Csányi Gábor Chlopicki, Stefan Recchia, Fabio A. Borbély Attila (1978-) (kardiológus) Galajda Zoltán (1962-) (szívsebész, érsebész) Édes István (1952-) (kardiológus) Velden, Jolanda, van der Stienen, Ger J. M. Papp Zoltán (1965-) (kardiológus, élettanász)
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5.

001-es BibID:BIBFORM005633
Első szerző:Hertelendi Zita (orvos)
Cím:Oxidation of myofilament protein sulfhydryl groups reduces the contractile force and its Ca2+ sensitivity in human cardiomyocytes / Hertelendi, Z., Toth, A., Borbely, A., Galajda, Z., van der Velden, J., Stienen, G. J., Edes, I., Papp, Z.
Dátum:2008
ISSN:1557-7716 (Electronic)
Megjegyzések:This study sought to characterize the relation between the oxidation of protein sulfhydryl (SH) groups and Ca2+-activated force production in the human myocardium. Triton-permeabilized left ventricular cardiomyocytes from donor hearts were exposed to an oxidative (2,2'-dithiodipyridine, DTDP) agent in vitro, and the changes in isometric force, its Ca2+ sensitivity, the cross-bridge-sensitive rate constant of force redevelopment at saturating [Ca2+] (k(tr,max)), and protein SH oxidation were monitored. DTDP (0.1-10 mM for 2 min) oxidized the myocardial proteins and diminished the Ca2+-activated force with different concentration dependences (EC(50,SH) = 0.17 +/- 0.02 mM and EC(50,force) = 2.46 +/- 0.22 mM; mean +/- SEM). The application of 2.5 mM DTDP decreased the maximal Ca2+-activated force (to 64%), its Ca2+ sensitivity (DeltapCa(50) = 0.22 +/- 0.02), and the steepness of the Ca2+-force relation (n(Hill), from 2.01 +/- 0.08 to 1.76 +/- 0.08). These changes were paralleled by reductions in the free SH content of the proteins (to 15%) and in k(tr,max) (to 75%). SH-specific labeling identified SH oxidation of myosin light chain 1 and actin at DTDP concentrations at which the changes in the contractile parameters occurred. Our data suggest that SH oxidation in selected myofilament proteins diminishes the Ca2+-activated force and its Ca2+ sensitivity through an impaired Ca2+ regulation of the actin-myosin cycle in the human heart.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
2,2'-Dipyridyl
Adult
Blotting, Western
Calcium
Cell Shape
Cells, Cultured
Disulfides
Female
Humans
Immunoprecipitation
Male
Microfilaments
Middle Aged
Myocardial Contraction
Myocytes, Cardiac
Oxidation-Reduction
Proteins/chemistry
Sulfhydryl Compounds
Megjelenés:Antioxidants and Redox Signaling. - 10 : 7 (2008), p. 1175-1184. -
További szerzők:Tóth Attila (1971-) (biológus) Borbély Attila (1978-) (kardiológus) Galajda Zoltán (1962-) (szívsebész, érsebész) Velden, Jolanda, van der Stienen, Ger J. M. Édes István (1952-) (kardiológus) Papp Zoltán (1965-) (kardiológus, élettanász)
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6.

001-es BibID:BIBFORM065597
Első szerző:Papp Zoltán (kardiológus, élettanász)
Cím:Altered myocardial force generation in end-stage human heart failure / Zoltán Papp, Jolanda van der Velden, Attila Borbély, István Édes, Ger J. M. Stienen
Dátum:2014
ISSN:2055-5822
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:ESC Heart Failure. - 1 : 2 (2014), p. 160-165. -
További szerzők:Velden, Jolanda, van der Borbély Attila (1978-) (kardiológus) Édes István (1952-) (kardiológus) Stienen, Ger J. M.
Pályázati támogatás:TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Kardiológia Kutatócsoport
Health-2010; MEDIA-261409
FP7
4.2.4.A/2-11-1-2012-0001
TÁMOP
K 109083
OTKA
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7.

001-es BibID:BIBFORM030905
Első szerző:Papp Zoltán (kardiológus, élettanász)
Cím:Effects of Ca2+-sensitizers in permeabilized cardiac myocytes from donor and end-stage failing human hearts / Papp Z., van Der Velden J., Borbély A., Édes I., Stienen G. J. M.
Dátum:2004
Megjegyzések:During heart failure, alterations occur in contractile protein expression and phosphorylation, which may influence the effects of Ca2+ -sensitizers. To quantify the magnitude of these effects, isometric force was studied in mechanically isolated Triton-skinned myocytes from end-stage failing and non-failing donor hearts under control conditions (pH 7.2; no added inorganic phosphate (Pi)) and under mimicked ischemic conditions (pH 6.5; 10 mM Pi). Two different Ca2+ -sensitizers were used: EMD 53998 (10 microM), which exerts its influence through the actin-myosin interaction, and OR-1896 (10 microM) (the active metabolite of levosimendan), which affects the Ca2+ -sensory function of the thin filaments. The maximal force (Po) measured at saturating Ca2+ concentration and the resting force (Prest) determined in the virtual absence of Ca2+ (pCa 9) did not differ between the failing and non-failing myocytes, but the Ca2+ concentration required to induce the half-maximal force under control conditions was significantly lower in the failing than in the non-failing myocytes (DeltapCa50=0.15). This difference in Ca2+ -sensitivity, however, was abolished during mimicked ischemia. EMD 53998 increased Po and Prest by approximately 15% of Po and greatly enhanced the Ca2+ -sensitivity (DeltapCa50 > 0.25) of force production. OR-1896 did not affect Po and Prest, and provoked a small, but significant Ca2+ -sensitization (DeltapCa50 approximately 0.1). All of these effects were comparable in the donor and failing myocytes, but, in contrast with OR-1896, EMD 53998 considerably diminished the difference in the Ca2+ -sensitivities between the failing and non-failing myocytes. The action of Ca2+ -sensitizers under mimicked ischemic conditions was impaired to a similar degree in the donor and the failing myocytes. Our results indicate that the Ca2+ -activation of the myofibrillar system is altered in end-stage human heart failure. This modulates the effects of Ca2+ -sensitizers both under control and under mimicked ischemic conditions.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of Muscle Research and Cell Motility. - 25 : 3 (2004), p. 219-224. -
További szerzők:Velden, Jolanda, van der Borbély Attila (1978-) (kardiológus) Édes István (1952-) (kardiológus) Stienen, Ger J. M.
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