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1.

001-es BibID:BIBFORM057819
Első szerző:Csató Viktória (molekuláris biológus)
Cím:Hydrogen peroxide elicits constriction of skeletal muscle arterioles by activating the arachidonic acid pathway / Viktória Csató, Attila Pető, Ákos Koller, István Édes, Attila Tóth, Zoltán Papp
Dátum:2014
ISSN:1932-6203
Megjegyzések:Aims: The molecular mechanisms of the vasoconstrictor responses evoked by hydrogen peroxide (H2O2) have not been clearly elucidated in skeletal muscle arterioles. Methods and results: Changes in diameter of isolated, cannulated and pressurized gracilis muscle arterioles (GAs) of Wistar-Kyoto rats were determined under various test conditions. H2O2 (10-100 ?M) evoked concentration-dependent constrictions in the GAs, which were inhibited by endothelium removal, or by antagonists of phospholipase A (PLA; 100 ?M 7,7-dimethyl-(5Z,8Z)-eicosadienoic acid), protein kinase C (PKC; 10 ?M chelerythrine), phospholipase C (PLC; 10 ?M U-73122), or Src family tyrosine kinase (Src kinase; 1 ?M Src Inhibitor-1). Antagonists of thromboxane A2 (TXA2; 1 ?M SQ-29548) or the non-specific cyclooxygenase (COX) inhibitor indomethacin (10 ?M) converted constrictions to dilations. The COX-1 inhibitor (SC-560, 1 ?M) demonstrated a greater reduction in constriction and conversion to dilation than that of COX-2 (celecoxib, 3 ?M). H2O2 did not elicit significant changes in arteriolar Ca2+ levels measured with Fura-2. Conclusions: These data suggest that H2O2 activates the endothelial Src kinase/PLC/PKC/PLA pathway, ultimately leading to the synthesis and release of TXA2 by COX-1, thereby increasing the Ca2+ sensitivity of the vascular smooth muscle cells and eliciting constriction in rat skeletal muscle arterioles.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
hydrogen peroxide
phospholipase C
arachidonic acid
smooth muscle calcium
constrictions
Megjelenés:Plos One. - 9 : 8 (2014), p. 1-10. -
További szerzők:Pető Attila (1990-) (általános orvos) Koller Ákos Édes István (1952-) (kardiológus) Tóth Attila (1971-) (biológus) Papp Zoltán (1965-) (kardiológus, élettanász)
Pályázati támogatás:OTKA-K108444
OTKA
OTKA-K84300
OTKA
OTKA-K109083
OTKA
TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Kardiológia Kutatócsoport
SROP-4.2.2.A-11/1/KONV-2012-0017
Egyéb
SROP-4.2.2.A-11/1/KONV-2012-0024
Egyéb
Internet cím:Szerző által megadott URL
DOI
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2.

001-es BibID:BIBFORM048797
Első szerző:Czikora Ágnes (molekuláris biológus)
Cím:Different desensitization patterns for sensory and vascular TRPV1 populations in the rat : expression, localization and functional consequences / Ágnes Czikora, Ibolya Rutkai, Enikő T. Pásztor, Andrea Szalai, Róbert Pórszász, Judit Boczán, István Édes, Zoltán Papp, Attila Tóth
Dátum:2013
ISSN:1932-6203
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Plos One. - 8 : 11 (2013), p. 1-8. -
További szerzők:Rutkai Ibolya (1985-) (molekuláris biológus) Pásztorné Tóth Enikő (1966-) (laboratóriumi analitikus) Szalai Andrea (1968-) (analitikus) Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus) Boczán Judit (1972-) (neurológus) Édes István (1952-) (kardiológus) Papp Zoltán (1965-) (kardiológus, élettanász) Tóth Attila (1971-) (biológus)
Pályázati támogatás:TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
K84300
OTKA
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM050126
035-os BibID:Article ID: e87844
Első szerző:Fagyas Miklós (orvos)
Cím:New perspectives in the renin-angiotensin-aldosterone system (RAAS) III : endogenous inhibition of angiotensin converting enzyme (ACE) provides protection against cardiovascular diseases / Miklós Fagyas, Katalin Úri, Ivetta M. Siket, Andrea Daragó, Judit Boczán, Emese Bányai, István Édes, Zoltán Papp, Attila Tóth
Dátum:2014
ISSN:1932-6203
Megjegyzések:ACE inhibitor drugs decrease mortality by up to one-fifth in cardiovascular patients. Surprisingly, there are reports dating back to 1979 suggesting the existence of endogenous ACE inhibitors. Here we investigated the clinical significance of this potential endogenous ACE inhibition. ACE concentration and activity was measured in patient's serum samples (n=151). ACE concentration was found to be in a wide range (47-288 ng/mL). ACE activity decreased with the increasing concentration of the serum albumin (HSA): ACE activity was 56?1 U/L in the presence of 2.4?0.3 mg/mL HSA, compared to 39?1 U/L in the presence of 12?1 mg/mL HSA (values are mean?SEM). Effects of the differences in ACE concentration were suppressed in human sera: patients with ACE DD genotype exhibited a 64% higher serum ACE concentration (range, 74-288 ng/mL, median, 155.2 ng/mL, n=52) compared to patients with II genotype (range, 47-194 ng/mL, median, 94.5 ng/mL, n=28) while the difference in ACE activities was only 32% (range, 27.3-59.8 U/L, median, 43.11 U/L, and range 15.6-55.4 U/L, median, 32.74 U/L, respectively) in the presence of 12?1 mg/mL HSA. No correlations were found between serum ACE concentration (or genotype) and cardiovascular diseases, in accordance with the proposed suppressed physiological ACE activities by HSA (concentration in the sera of these patients: 48.5?0.5 mg/mL) or other endogenous inhibitors. Main implications are that (1) physiological ACE activity can be stabilized at a low level by endogenous ACE inhibitors, such as HSA; (2) angiotensin II elimination may have a significant role in angiotensin II related pathologies.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
ACE
HSA
endogenous ACE inhibition
angiotensin-converting enzyme
Molekuláris Medicina
Megjelenés:Plos One. - 9 : 4 (2014), p. 1-29. -
További szerzők:Úri Katalin Mányiné Siket Ivetta (1962-) (laborasszisztens) Daragó Andrea (1972-) (orvos, kardiológus) Boczán Judit (1972-) (neurológus) Bányai Emese (1984-) (orvos) Édes István (1952-) (kardiológus) Papp Zoltán (1965-) (kardiológus, élettanász) Tóth Attila (1971-) (biológus)
Pályázati támogatás:OTKA-K84300
OTKA
TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Vaszkuláris tranziens receptor potenciál (TRP) csatornák
TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Kardiológia Kutatócsoport
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM050118
035-os BibID:Article ID: e87843
Első szerző:Fagyas Miklós (orvos)
Cím:New perspectives in the renin-angiotensin-aldosterone system (RAAS) I : endogenous angiotensin converting enzyme (ACE) inhibition / Miklós Fagyas, Katalin Úri, Ivetta M. Siket, Andrea Daragó, Judit Boczán, Emese Bányai, István Édes, Zoltán Papp, Attila Tóth
Dátum:2014
ISSN:1932-6203
Megjegyzések:Angiotensin-converting enzyme (ACE) inhibitors represent the fifth most often prescribed drugs. ACE inhibitors decrease 5-year mortality by approximately one-fifth in cardiovascular patients. Surprisingly, there are reports dating back to 1979 suggesting the existence of endogenous ACE inhibitors, which endogenous inhibitory effects are much less characterized than that for the clinically administered ACE inhibitors. Here we aimed to investigate this endogenous ACE inhibition in human sera. It was hypothesized that ACE activity is masked by an endogenous inhibitor, which dissociates from the ACE when its concentration decreases upon dilution. ACE activity was measured by FAPGG hydrolysis first. The specific (dilution corrected) enzyme activities significantly increased by dilution of human serum samples (23.2?0.7U/L at 4-fold dilution, 51.4?0.3U/L at 32-fold dilution, n=3, p=0.001), suggesting the presence of an endogenous inhibitor. In accordance, specific enzyme activities did not changed by dilution when purified renal ACE was used, where no endogenous inhibitor was present (655?145U/L, 605?42U/L, n=3, p=0.715, respectively). FAPGG conversion strongly correlated with angiotensin I conversion suggesting that this feature is not related to the artificial substrate. Serum samples were ultra-filtered to separate ACE (MW: 180 kDa) and the hypothesized inhibitor. Filtering through 50 kDa filters was without effect, while filtering through 100 kDa filters eliminated the inhibiting factor (ACE activity after <100 kDa filtering: 56.4?2.4U/L, n=4, control: 26.4?0.7U/L, n=4, p<0.001). Lineweaver-Burk plot indicated non-competitive inhibition of ACE by this endogenous factor. The endogenous inhibitor had higher potency on the C-terminal active site than N-terminal active site of ACE. Finally, this endogenous ACE inhibition was also present in mouse, donkey, goat, bovine sera besides men (increasing of specific ACE activity from 4-fold to 32-fold dilution: 2.8-fold, 1.7-fold, 1.5-fold, 1.8-fold, 2.6-fold, respectively). We report here the existence of an evolutionary conserved mechanism suppressing circulating ACE activity, in vivo, similarly to ACE inhibitory drugs.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
ACE
angiotensin-converting enzyme
renin-angiotensin-aldosterone system
endogenous ACE inhibition
Molekuláris Medicina
Megjelenés:Plos One. - 9 : 4 (2014), p. 1-29. -
További szerzők:Úri Katalin Mányiné Siket Ivetta (1962-) (laborasszisztens) Daragó Andrea (1972-) (orvos, kardiológus) Boczán Judit (1972-) (neurológus) Bányai Emese (1984-) (orvos) Édes István (1952-) (kardiológus) Papp Zoltán (1965-) (kardiológus, élettanász) Tóth Attila (1971-) (biológus)
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Vaszkuláris tranziens receptor potenciál (TRP) csatornák
TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Kardiológia Kutatócsoport
K84300
OTKA
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

5.

001-es BibID:BIBFORM050119
035-os BibID:Article ID: e87844
Első szerző:Fagyas Miklós (orvos)
Cím:New perspectives in the renin-angiotensin-aldosterone system (RAAS) II : albumin suppresses angiotensin converting enzyme (ACE) activity in human / Miklós Fagyas, Katalin Úri, Ivetta M. Siket, Gábor Á. Fülöp, Viktória Csató, Andrea Daragó, Judit Boczán, Emese Bányai, István Elek Szentkirályi, Tamás Miklós Maros, Tamás Szerafin, István Édes, Zoltán Papp, Attila Tóth
Dátum:2014
ISSN:1932-6203
Megjegyzések:About 8% of the adult population is taking angiotensin-converting enzyme (ACE) inhibitors to treat cardiovascular disease including hypertension, myocardial infarction and heart failure. These drugs decrease mortality by up to one-fifth in these patients. We and others have reported previously that endogenous inhibitory substances suppress serum ACE activity, in vivo, similarly to the ACE inhibitor drugs. Here we have made an effort to identify this endogenous ACE inhibitor substance. ACE was crosslinked with interacting proteins in human sera. The crosslinked products were immunoprecipitated and subjected to Western blot. One of the crosslinked products was recognized by both anti-ACE and anti-HSA (human serum albumin) antibodies. Direct ACE-HSA interaction was confirmed by binding assays using purified ACE and HSA. HSA inhibited human purified (circulating) and human recombinant ACE with potencies (IC50) of 5.7?0.7 and 9.5?1.1 mg/mL, respectively. Effects of HSA on the tissue bound native ACE were tested on human saphenous vein samples. Angiotensin I evoked vasoconstriction was inhibited by HSA in this vascular tissue (maximal force with HSA: 6.14?1.34 mN, without HSA: 13.54?2.63 mN), while HSA was without effects on angiotensin II mediated constrictions (maximal force with HSA: 18.73?2.17 mN, without HSA: 19.22?3.50 mN).The main finding of this study is that HSA was identified as a potent physiological inhibitor of the ACE. The enzymatic activity of ACE appears to be almost completely suppressed by HSA when it is present in its physiological concentration. These data suggest that angiotensin I conversion is limited by low physiological ACE activities, in vivo.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
ACE
Renin-angiotensin-aldosterone system
human serum albumin
endogenous ACE inhibition
Molekuláris Medicina
Megjelenés:Plos One. - 9 : 4 (2014), p. 1-28. -
További szerzők:Úri Katalin Mányiné Siket Ivetta (1962-) (laborasszisztens) Fülöp Gábor Áron (1988-) (általános orvos) Csató Viktória (1986-) (molekuláris biológus) Daragó Andrea (1972-) (orvos, kardiológus) Boczán Judit (1972-) (neurológus) Bányai Emese (1984-) (orvos) Szentkirályi István (1970-) (szívsebész) Maros Tamás Miklós (1969-) (szívsebész) Szerafin Tamás (1960-) (szívsebész, mellkassebész) Édes István (1952-) (kardiológus) Papp Zoltán (1965-) (kardiológus, élettanász) Tóth Attila (1971-) (biológus)
Pályázati támogatás:TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Kardiológia Kutatócsoport
TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Vaszkuláris tranziens receptor potenciál (TRP) csatornák
K84300
OTKA
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

6.

001-es BibID:BIBFORM050127
035-os BibID:Article ID: e87845
Első szerző:Úri Katalin
Cím:New perspectives in the renin-angiotensin-aldosterone system (RAAS) IV : circulating ACE2 as a biomarker of systolic dysfunction in human hypertension and heart failure / Katalin Úri, Miklós Fagyas, Ivetta Mányiné Siket, Attila Kertész, Zoltán Csanádi, Gábor Sándorfi, Marcell Clemens, Roland Fedor, Zoltán Papp, István Édes, Attila Tóth, Erzsébet Lizanecz
Dátum:2014
ISSN:1932-6203
Megjegyzések:Background. Growing evidence exists for soluble Angiotensin Converting Enzyme-2 (sACE2) as a biomarker in definitive heart failure (HF), but there is little information about changes in sACE2 activity in hypertension with imminent heart failure and in reverse remodeling. Methods, Findings. Patients with systolic HF (NYHAII-IV, enrolled for cardiac resynchronisation therapy, CRT, n=100) were compared to hypertensive patients (n=239) and to a healthy cohort (n=45) with preserved ejection fraction (EF>50%) in a single center prospective clinical study. The status of the heart failure patients were checked before and after CRT. Biochemical (ACE and sACE2 activity, ACE concentration) and echocardiographic parameters (EF, left ventricular end-diastolic (EDD) and end-systolic diameter (ESD) and dP/dt) were measured. sACE2 activity negatively correlated with EF and positively with ESD and EDD in all patient's populations, while it was independent in the healthy cohort. sACE2 activity was already increased in the hypertensive group, where signs for imminent heart failure (slightly decreased EF and barely increased NT-proBNP levels) were detected. sACE2 activities further increased in patients with definitive heart failure (EF<50%), while sACE2 activities decreased with the improvement of the heart failure after CRT (reverse remodeling). Serum angiotensin converting enzyme (ACE) concentrations were lower in the diseased populations, but did not show a strong correlation with the echocardiographic parameters.Conclusions. Soluble ACE2 activity appears to be biomarker in heart failure, and in hypertension, where heart failure may be imminent. Our data suggest that sACE2 is involved in the pathomechanism of hypertension and HF.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
ACE2
angiotensin-converting enzyme 2
heart failure
hypertension
Megjelenés:Plos One. - 9 : 4 (2014), p. 1-32. -
További szerzők:Fagyas Miklós (1984-) (orvos) Mányiné Siket Ivetta (1962-) (laborasszisztens) Kertész Attila Béla (1973-) (kardiológus) Csanádi Zoltán (1960-) (kardiológus) Sándorfi Gábor (1976-) (belgyógyász, kardiológus) Clemens Marcell (1979-) (kardiológus) Fedor Roland (1975-) (sebész) Papp Zoltán (1965-) (kardiológus, élettanász) Édes István (1952-) (kardiológus) Tóth Attila (1971-) (biológus) Lizanecz Erzsébet (1978-) (orvos)
Pályázati támogatás:TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Kardiológia Kutatócsoport
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
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7.

001-es BibID:BIBFORM044733
Első szerző:Vandenwijngaert, Sara
Cím:Increased Cardiac Myocyte PDE5 Levels in Human and Murine Pressure Overload Hypertrophy Contribute to Adverse LV Remodeling / Sara Vandenwijngaert, Pokreisz Péter, Hadewich Hermans, Hilde Gillijns, Marijke Pellens, Noortje A. M. Bax, Giulia Coppiello, Wouter Oosterlinck, Balogh Ágnes, Papp Zoltán, Carlijn V. C. Bouten, Jozef Bartunek, Jan D'hooge, Aernout Luttun, Erik Verbeken, Marie Christine Herregods, Paul Herijgers, Kenneth D. Bloch, Stefan Janssens
Dátum:2013
ISSN:1932-6203
Megjegyzések:BACKGROUND: The intracellular second messenger cGMP protects the heart under pathological conditions. We examined expression of phosphodiesterase 5 (PDE5), an enzyme that hydrolyzes cGMP, in human and mouse hearts subjected to sustained left ventricular (LV) pressure overload. We also determined the role of cardiac myocyte-specific PDE5 expression in adverse LV remodeling in mice after transverse aortic constriction (TAC). METHODOLOGY/PRINCIPAL FINDINGS: In patients with severe aortic stenosis (AS) undergoing valve replacement, we detected greater myocardial PDE5 expression than in control hearts. We observed robust expression in scattered cardiac myocytes of those AS patients with higher LV filling pressures and BNP serum levels. Following TAC, we detected similar, focal PDE5 expression in cardiac myocytes of C57BL/6NTac mice exhibiting the most pronounced LV remodeling. To examine the effect of cell-specific PDE5 expression, we subjected transgenic mice with cardiac myocyte-specific PDE5 overexpression (PDE5-TG) to TAC. LV hypertrophy and fibrosis were similar as in WT, but PDE5-TG had increased cardiac dimensions, and decreased dP/dtmax and dP/dtmin with prolonged tau (P<0.05 for all). Greater cardiac dysfunction in PDE5-TG was associated with reduced myocardial cGMP and SERCA2 levels, and higher passive force in cardiac myocytes in vitro. CONCLUSIONS/SIGNIFICANCE: Myocardial PDE5 expression is increased in the hearts of humans and mice with chronic pressure overload. Increased cardiac myocyte-specific PDE5 expression is a molecular hallmark in hypertrophic hearts with contractile failure, and represents an important therapeutic target.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Plos One. - 8 : 3 (2013), p. 1-9. -
További szerzők:Pokreisz Péter Hermans, Hadewich Gillijns, Hilde Pellens, Marijke Bax, Noortje A. M. Coppiello, Giulia Oosterlinck, Wouter Balogh Ágnes (1984-) (kardiológus) Papp Zoltán (1965-) (kardiológus, élettanász) Bouten, Carlijn V. C. Bartunek, Jozef D'hooge, Jan Luttun, Aernout Verbeken, Erik Herregods, Marie Christine Herijgers, Paul Bloch, Kenneth D. Janssens, Stefan
Pályázati támogatás:TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
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