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001-es BibID:BIBFORM089749
035-os BibID:(cikkazonosító)8172 (scopus)85094855183 (wos)000588924400001
Első szerző:Alvarado, Gerardo
Cím:Heme-Induced Oxidation of Cysteine Groups of Myofilament Proteins Leads to Contractile Dysfunction of Permeabilized Human Skeletal Muscle Fibres / Alvarado Gerardo, Tóth Attila, Csősz Éva, Kalló Gergő, Dankó Katalin, Csernátony Zoltán, Smith Ann, Gram Magnus, Akerström Bo, Édes István, Balla György, Papp Zoltán, Balla József
Dátum:2020
ISSN:1661-6596 1422-0067
Megjegyzések:Heme released from red blood cells targets a number of cell components including the cytoskeleton. The purpose of the present study was to determine the impact of free heme (20?300 ?M) on human skeletal muscle fibres made available during orthopedic surgery. Isometric force production and oxidative protein modifications were monitored in permeabilized skeletal muscle fibre segments. A single heme exposure (20 ?M) to muscle fibres decreased Ca2+-activated maximal (active) force (Fo) by about 50% and evoked an approximately 3-fold increase in Ca2+-independent (passive) force (Fpassive). Oxidation of sulfhydryl (SH) groups was detected in structural proteins (e.g., nebulin, ?-actinin, meromyosin 2) and in contractile proteins (e.g., myosin heavy chain and myosin-binding protein C) as well as in titin in the presence of 300 ?M heme. This SH oxidation was not reversed by dithiothreitol (50 mM). Sulfenic acid (SOH) formation was also detected in the structural proteins (nebulin, ?-actinin, meromyosin). Heme effects on SH oxidation and SOH formation were prevented by hemopexin (Hpx) and ?1-microglobulin (A1M). These data suggest that free heme has a significant impact on human skeletal muscle fibres, whereby oxidative alterations in structural and contractile proteins limit contractile function. This may explain and or contribute to the weakness and increase of skeletal muscle stiffness in chronic heart failure, rhabdomyolysis, and other hemolytic diseases. Therefore, therapeutic use of Hpx and A1M supplementation might be effective in preventing heme-induced skeletal muscle alterations.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
skeletal muscle fibre
contractile dysfunction
heme
sulfhydryl groups
sulfenic acid formation
chronic heart failure
oxidation; hemopexin
[alfa]1-microglobulin
skeletal muscle myopathy
Megjelenés:International Journal Of Molecular Sciences. - 21 : 21 (2020), p. 1-17. -
További szerzők:Tóth Attila (1971-) (biológus) Csősz Éva (1977-) (biokémikus, molekuláris biológus) Kalló Gergő (1989-) (molekuláris biológus) Dankó Katalin (1952-2021) (belgyógyász, allergológus és klinikai immunológus) Csernátony Zoltán (1959-2023) (ortopéd sebész, traumatológus) Smith, Ann Gram, Magnus Akerström, Bo Édes István (1952-) (kardiológus) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Papp Zoltán (1965-) (kardiológus, élettanász) Balla József (1959-) (belgyógyász, nephrológus)
Pályázati támogatás:EFOP-3.6.2-16-2017-00006
EFOP
OTKA-K-132828
OTKA
K-84300
OTKA
K-109083
OTKA
GINOP-2.3.2-15-2016-00043
GINOP
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2.

001-es BibID:BIBFORM060830
Első szerző:Alvarado, Gerardo
Cím:Heme-induced contractile dysfunction in Human cardiomyocytes caused by oxidant damage to thick filament proteins / Gerardo Alvarado, Viktória Jeney, Attila Tóth, Éva Csősz, Gergő Kalló, An T. Huynh, Csaba Hajnal, Judit Kalász, Enikő T. Pásztor, István Édes, Magnus Gram, Bo Akerström, Ann Smith, John W. Eaton, György Balla, Zoltán Papp, József Balla
Dátum:2015
ISSN:0891-5849
Megjegyzések:Intracellular free heme predisposes to oxidant-mediated tissue damage. We hypothesized that free heme causes alterations in myocardial contractility via disturbed structure and/or regulation of the contractile proteins. Isometric force production and its Ca2þ-sensitivity (pCa50) were monitored in permeabilized human ventricular cardiomyocytes. Heme exposure altered cardiomyocyte morphology and evoked robust decreases in Ca2þ-activated maximal active force (Fo) while increasing Ca2þ-independent passive force (Fpassive). Heme treatments, either alone or in combination with H2O2, did not affect pCa50. The increase in Fpassive started at 3 mM heme exposure and could be partially reversed by the antioxidant dithiothreitol. Protein sulfhydryl (SH) groups of thick myofilament content decreased and sulfenic acid formation increased after treatment with heme. Partial restoration in the SH group content was observed in a protein running at 140 kDa after treatment with dithiothreitol, but not in other proteins, such as filamin C, myosin heavy chain, cardiac myosin binding protein C, and α-actinin. Importantly, binding of heme to hemopexin or alpha-1-microglobulin prevented its effects on cardiomyocyte contractility, suggesting an allosteric effect. In line with this, free heme directly bound to myosin light chain 1 in human cardiomyocytes. Our observations suggest that free heme modifies cardiac contractile proteins via posttranslational protein modifications and via binding to myosin light chain 1, leading to severe contractile dysfunction. This may contribute to systolic and diastolic cardiac dysfunctions in hemolytic diseases, heart failure, and myocardial ischemia-reperfusion injury.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Cardiomyocyte
Contractile function
Heme
Calcium sensitivity
Myosin light chain 1
Cardiac myosin binding protein C
Myosin heavy chain
Titin
H2O2
Sulfenic acid Oxidation
Megjelenés:Free Radical Biology And Medicine. - 89 (2015), p. 248-262. -
További szerzők:Jeney Viktória (1971-) (vegyész, kémia tanár) Tóth Attila (1971-) (biológus) Csősz Éva (1977-) (biokémikus, molekuláris biológus) Kalló Gergő (1989-) (molekuláris biológus) Huynh, An T. Hajnal Csaba Kalász Judit (1986-) (molekuláris biológus) Pásztorné Tóth Enikő (1966-) (laboratóriumi analitikus) Édes István (1952-) (kardiológus) Gram, Magnus Akerström, Bo Smith, Ann Eaton, John W. Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Papp Zoltán (1965-) (kardiológus, élettanász) Balla József (1959-) (belgyógyász, nephrológus)
Pályázati támogatás:TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Kardiológia Kutatócsoport
TÁMOP-4.2.2/B-10/1-2010-0024
TÁMOP
Laki Kálmán Doktori Iskola
84300
OTKA
109083
OTKA
112333
OTKA
MTA-DE
MTA
Vascularis Biológia, Thrombosis-Haemostasis Kutatócsoport
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Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM049848
Első szerző:Balogh Ágnes (kardiológus)
Cím:Myofilament carbonylation modulates contractility in human cardiomyocytes / Ágnes Balogh, Attila Tóth, Enikő Pásztorné Tóth, László Nagy, Árpád Kovács, Judit Kalász, Gerardo Alvarado Contreras, István Édes, Zoltán Papp
Dátum:2014
Megjegyzések:This study investigated the effects of myofilament carbonylation in permeabilized human left ventricular cardiomyocytes. Protein carbonylation was monitored by the oxyblot method following the in vitro application of the Fenton reaction reagents [iron(II), ascorbic acid and hydrogen peroxide (H2O2)], known to produce hydroxyl radicals. Sulfhydryl group oxidation was assessed in parallel by the Ellman assay. During force measurements, the Ca2+-activated active force, the Ca2+-independent passive force and the Ca2+ sensitivity of force production (pCa50) were measured in permeabilized cardiomyocytes before and after in vitro carbonylation. Carbonylation at the levels of several myofilament proteins (e.g. myosin heavy chain, ?-actinin, actin, myosin binding protein C, desmin and myosin light chain 1) was enhanced by increasing concentrations of H2O2 (0-105 ?M) in the Fenton solution. Carbonylation suspended active force generation following aggressive Fenton treatment (105 ?M H2O2), whereas the application of 3*103 ?M H2O2 decreased pCa50 (from 5.74?0.01 to 5.65?0.01; mean?SEM, P<0.05) and increased the passive force (from 1.72?0.21 kN/m2 to 2.33?0.22 kN/m2). None of these changes was influenced by sulfhydryl group reduction. Thus, myofilament carbonylation dysregulates the contractile function in human cardiomyocytes, and may therefore mediate the contractile dysfunction during oxidative stress.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Experimental & Clinical Cardiology 20 : 1 (2014), p. 2026-2035. -
További szerzők:Tóth Attila (1971-) (biológus) Pásztorné Tóth Enikő (1966-) (laboratóriumi analitikus) Nagy László (1988-) (orvos) Kovács Árpád (1986-) (kardiológus) Kalász Judit (1986-) (molekuláris biológus) Contreras, Gerardo Alvarado (1978-) (orvos) Édes István (1952-) (kardiológus) Papp Zoltán (1965-) (kardiológus, élettanász)
Pályázati támogatás:TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Kardiológia Kutatócsoport
K 109083
OTKA
HEALTH-2010: "MEDIA-Metabolic Road to Diastolic Heart Failure" MEDIA-261409
FP7
TÁMOP 4.2.4. A/2-11-1-2012-0001
TÁMOP
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM049141
Első szerző:Balogh Ágnes (kardiológus)
Cím:Myofilament protein carbonylation contributes to the contractile dysfunction in the infarcted LV region of mouse hearts / Ágnes Balogh, David Santer, Enikő T. Pásztor, Attila Tóth, Dániel Czuriga, Bruno K. Podesser, Karola Trescher, Kornelia Jaquet, Ferenc Erdődi, István Édes, Zoltán Papp
Dátum:2014
ISSN:0008-6363
Megjegyzések:Aims: The region-specific mechanical function of left ventricular (LV) murinecardiomyocytes and the role of phosphorylation and oxidative modifications of myofilamentproteins were investigated in the process of post-myocardial infarction (MI) remodeling 10weeks after ligation of the left anterior descending (LAD) coronary artery. Methods andResults: Permeabilized murine cardiomyocytes from the remaining anterior and a remotenoninfarcted inferior LV area were compared with those of noninfarcted age-matchedcontrols. Myofilament phosphorylation, sulfhydryl (SH) oxidation and carbonylation werealso assayed. The Ca2+ sensitivity of force production was significantly lower in the anteriorwall (pCa50:5.81?0.03, mean?SEM, at 2.3 ?m sarcomere length) than that in the controls(pCa50:5.91?0.02) or in the MI inferior area (pCa50:5.88?0.02). The level of troponin Iphosphorylation was lower and that of myofilament protein SH oxidation was higher in theanterior location relative to controls, but these changes did not explain the differences in Ca2+sensitivities. On the other hand, significantly higher carbonylation levels [e.g. in myosinheavy chain (MHC) and actin] were observed in the MI anterior wall [carbonylation index(CI), CIMHC:2.06?0.46, CIactin:1.46?0.18] than in the controls (CI:1). In vitro Fenton-basedmyofilament carbonylation in the control cardiomyocytes also decreased the Ca2+ sensitivityof force production irrespective of the phosphorylation status of the myofilaments.Furthermore, the Ca2+ sensitivity correlated strongly with myofilament carbonylation levels inall investigated samples. Conclusions: Post-MI myocardial remodeling involves increasedmyofibrillar protein carbonylation and decreased Ca2+ sensitivity of force production, leadingpotentially to contractile dysfunction in the remaining cardiomyocytes of the infarcted area.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Molekuláris Medicina
contractile function
infarction
myocytes
remodeling
sarcomere
Megjelenés:Cardiovascular Research. - 101 : 1 (2014), p. 108-119. -
További szerzők:Santer, David Pásztorné Tóth Enikő (1966-) (laboratóriumi analitikus) Tóth Attila (1971-) (biológus) Czuriga Dániel (1982-) (kardiológus) Podesser, Bruno Karl Trescher, Karola Jaquet, Kornelia Erdődi Ferenc (1953-) (biokémikus) Édes István (1952-) (kardiológus) Papp Zoltán (1965-) (kardiológus, élettanász)
Pályázati támogatás:TÁMOP-4.2.2/B-10/1-2010-0024
TÁMOP
TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
K 109083
OTKA
TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Biomolekuláris interakciók jellemzőinek kvantitatív meghatározása
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Szerző által megadott URL
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Intézményi repozitóriumban (DEA) tárolt változat
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5.

001-es BibID:BIBFORM095647
035-os BibID:(cikkazonosító)1708 (WoS)000676633500001 (Scopus)85114067373
Első szerző:Bánhegyi Viktor (kardiológus)
Cím:Human Tissue Angiotensin Converting Enzyme (ACE) Activity Is Regulated by Genetic Polymorphisms, Posttranslational Modifications, Endogenous Inhibitors and Secretion in the Serum, Lungs and Heart / Viktor Bánhegyi, Attila Enyedi Gábor Áron Fülöp, Attila Oláh, Ivetta Mányiné Siket, Csongor Váradi, Klaudia Bottyán, Mária Lódi, Alexandra Csongrádi, Azeem J. Umar, Miklós Fagyas, Dániel Czuriga, István Édes, Miklós Pólos, Béla Merkely, Zoltán Csanádi, Zoltán Papp, Gábor Szabó, Tamás Radovits, István Takács, Attila Tóth
Dátum:2021
ISSN:2073-4409
Megjegyzések:Objective: Inhibitors of the angiotensin converting enzyme (ACE) are the primarily chosen drugs to treat heart failure and hypertension. Moreover, an imbalance in tissue ACE/ACE2 activity is implicated in COVID-19. In the present study, we tested the relationships between circulating and tissue (lung and heart) ACE levels in men. Methods: Serum, lung (n = 91) and heart (n = 72) tissue samples were collected from Caucasian patients undergoing lung surgery or heart transplantation. ACE I/D genotype, ACE concentration and ACE activity were determined from serum and tissue samples. Clinical parameters were also recorded. Results: A protocol for ACE extraction was developed for tissue ACE measurements. Extraction of tissue-localized ACE was optimal in a 0.3% Triton-X-100 containing buffer, resulting in 260 ? 12% higher ACE activity over detergent-free conditions. SDS or higher Triton-X-100 concentrations inhibited the ACE activity. Serum ACE concentration correlated with ACE I/D genotype (II: 166 ? 143 ng/mL, n = 19, ID: 198 ? 113 ng/mL, n = 44 and DD: 258 ? 109 ng/mL, n = 28, p < 0.05) as expected. In contrast, ACE expression levels in the lung tissue were approximately the same irrespective of the ACE I/D genotype (II: 1423 ? 1276 ng/mg, ID: 1040 ? 712 ng/mg and DD: 930 ? 1273 ng/mg, p > 0.05) in the same patients (values are in median ? IQR). Moreover, no correlations were found between circulating and lung tissue ACE concentrations and activities (Spearman's p > 0.05). In contrast, a significant correlation was identified between ACE activities in serum and heart tissues (Spearman's Rho = 0.32, p < 0.01). Finally, ACE activities in lung and the serum were endogenously inhibited to similar degrees (i.e., to 69 ? 1% and 53 ? 2%, respectively). Conclusion: Our data suggest that circulating ACE activity correlates with left ventricular ACE, but not with lung ACE in human. More specifically, ACE activity is tightly coordinated by genotype-dependent expression, endogenous inhibition and secretion mechanisms.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
angiotenzin konvertáló enzim
szív
tüdő
reguláció
szöveti
keringő
Megjelenés:Cells. - 10 : 7 (2021), p. 1-13. -
További szerzők:Enyedi Attila (1975-) (sebész) Fülöp Gábor Áron (1988-) (általános orvos) Oláh Attila (sebész) Mányiné Siket Ivetta (1962-) (laborasszisztens) Váradi Csongor (1984-) (sebész, mellkassebész szakorvos) Bottyán Klaudia Lódi Mária (1991-) Csongrádi Alexandra (1990-) (molekuláris biológus) Umar, Muhammad Azeem Jalil Fagyas Miklós (1984-) (orvos) Czuriga Dániel (1982-) (kardiológus) Édes István (1952-) (kardiológus) Pólos Miklós Merkely Béla (1965-) (orvos) Csanádi Zoltán (1960-) (kardiológus) Papp Zoltán (1965-) (kardiológus, élettanász) Szabó Gábor (orvos) Radovits Tamás Takács István (1963-) (sebész) Tóth Attila (1971-) (biológus)
Pályázati támogatás:GINOP-2.2.1-15-2017-00043
GINOP
ÚNKP-18-3-III-DE-209
Egyéb
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6.

001-es BibID:BIBFORM015742
Első szerző:Barta Judit (kardiológus)
Cím:Calpain-1-sensitive myofibrillar proteins of the human myocardium / Barta Judit, Tóth Attila, Édes István, Vaszily Miklós, Papp Gy. Julius, Varró András, Papp Zoltán
Dátum:2005
Megjegyzések:Calpain-1 is a ubiquitous intracellular Ca2+-activated protease, which has been implicated in the pathogenesis of reversible myocardial depression (i.e. myocardial stunning) that follows ischemia and reperfusion via myofibrillar protein degradation. However, the target proteins of this degradative process in the human myocardium have not yet been identified. In order to compare the levels of Calpain-1 susceptibility within a set of human myofibrillar proteins (titin, alpha-fodrin, desmin, troponin T (cTnT), troponin I (cTnI) and alpha-actinin), crude left ventricular tissue homogenates were incubated for 0.5, 15, 30, 60 or 120 min in the presence of Calpain-1 (1 U or 5 U). Differences in the kinetics and extents of protein degradation were subsequently evaluated by using silver-stained SDS-polyacrylamide gels and Western immunoblot analyses. These assays revealed myofibrillar proteins with high (titin and alpha-fodrin), moderate (desmin and cTnT), or low (cTnI and alpha-actinin) relative Calpain-1 susceptibilities. The level of phosphorylation of cTnI did not explain its relatively low Calpain-1 susceptibility. Moreover, the molecular mass distributions of the truncated alpha-fodrin, desmin and cTnI fragments resulting from Ca2+-dependent autoproteolysis exhibited marked similarities with those of their Calpain-1-clipped products. These in vitro results shed light on a number of structural (titin, alpha-fodrin, desmin and alpha-actinin) and regulatory (cTnT and cTnI) proteins within the contractile apparatus as potential targets of Calpain-1. Their degradation may contribute to the development of postischemic stunning in the human myocardium.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
calpain
desmin
stunning
titin
troponin I
troponin T
Megjelenés:Molecular and Cellular Biochemistry. - 278 : 1-2 (2005), p. 1-8. -
További szerzők:Tóth Attila (1971-) (biológus) Édes István (1952-) (kardiológus) Vaszily Miklós (1949-) (szívsebész) Papp Gy. Julius (Szeged) Varró András (1954-) (farmakológus, klinikai farmakológus) Papp Zoltán (1965-) (kardiológus, élettanász)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
Borító:

7.

001-es BibID:BIBFORM015741
Első szerző:Barta Judit (kardiológus)
Cím:Calpain-1-dependent degradation of troponin I mutants found in familial hypertrophic cardiomyopathy / Barta Judit, Tóth Attila, Jaquet Kornelia, Redlich Alexander, Édes István, Papp Zoltán
Dátum:2003
Megjegyzések:The mechanism by which mutations of the cardiac troponin I (cTnI) gene evoke familial hypertrophic cardiomyopathy (fHCM)is unknown. In this investigation the potential effects of three fHCM-related cTnI mutations on Calpain-1-induced cTnI degradation were tested, and a study was made of whether additional conformational changes due to troponin complex formation and protein kinase A-induced phosphorylation affect the intensity of cTnI proteolysis. Purified recombinant wild-type cTnI and three of its fHCM-related missense mutants (R145G, G203S and K206Q), alone or in the troponin complex (i.e. together with troponin C and troponin T), in the non-phosphorylated or protein kinase A-bisphosphorylated forms were proteolyzed invitro in the presence of Calpain-1 (0.05?2.5 U) at 30?C. Following incubation with Calpain-1 for 0.5, 30, 60 or 120 min, the extent of protein degradation was evaluated through the use of Western immunoblotting and densitometry. The results indicated that both the wild-type and the mutant cTnI molecules were susceptible to Calpain-1. However, the degradation of the cTnI molecules in the troponin complex was less intense than that of the non-complexed forms. Moreover, phosphorylation by protein kinase A conferred effective protection against cTnI proteolysis. The data suggested that mutations in the central inhibitory domain (R145G) and in the C-terminal region (G203S and K206Q) of cTnI do not affect its Calpain-1-mediated degradation, or the phosphorylation-induced protection against proteolysis.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
hypertrophic cardiomyopathy
calpain
troponin I
mutation
Megjelenés:Molecular and Cellular Biochemistry. - 251 : 1-2 (2003), p. 83-88. -
További szerzők:Tóth Attila (1971-) (biológus) Jaquet, Kornelia Redlich, Alexander Édes István (1952-) (kardiológus) Papp Zoltán (1965-) (kardiológus, élettanász)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
Borító:

8.

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)
Internet cím:elektronikus változat
DOI
Borító:

9.

001-es BibID:BIBFORM057849
Első szerző:Csató Viktória (molekuláris biológus)
Cím:Myeloperoxidase evokes substantial vasomotor responses in isolated skeletal muscle arterioles of the rat / Viktória Csató, Attila Pető, Gábor Áron Fülöp, Ibolya Rutkai, Enikő Pásztorné T., Miklós Fagyas, Judit Kalász, István Édes, Attila Tóth, Zoltán Papp
Dátum:2015
ISSN:1748-1708
Megjegyzések:Aims: Myeloperoxidase (MPO) catalyzes the formation of a wide variety of oxidants,including hypochlorous acid (HOCl), and contributes to cardiovascular diseaseprogression. We hypothesized that during its action MPO evokes substantionalvasomotor responses.Methods: Following exposure to MPO (1.92 mU ml-1) in the presence of increasingconcentrations of hydrogen peroxide (H2O2) changes in arteriolar diameter of isolatedgracilis skeletal muscle arterioles (SMAs), and coronary arterioles (CAs) and in theisometric force in basilar arteries (BAs) of the rat were monitored.Results: MPO increased vascular tone to different degrees in CAs, SMAs and BAs.The mechanism of increased vasoconstriction was studied in detail in SMAs. MPO-evoked vasoconstrictions were prevented by the MPO inhibitor 4-aminobenzhydrazide (50 ?M), by endothelium removal in the SMAs. Surprisingly, theHOCl scavenger L-methionine (100 ?M), the thromboxane A2 (TXA2) antagonist SQ-29548 (1 ?M) or the nonspecific cyclooxygenase (COX) antagonist indomethacin (1?M) converted the MPO-evoked vasoconstrictions to pronounced vasodilations inSMAs; not seen in the presence of H2O2. In contrast to norepinephrine-inducedvasoconstrictions, the MPO-evoked vasoconstrictions were not accompanied bysignificant increases in arteriolar [Ca2+ 44 ] levels in SMAs.Conclusion: These data showed, H2O2-derived HOCl to be a potent vasoconstrictorupon MPO application. HOCl activated the COX pathway, causing the synthesis andrelease of TXA2-like substance to increase the Ca2+ 47 sensitivity of the contractileapparatus in vascular smooth muscle cells and thereby to augment H2O2-evokedvasoconstrictions. Nevertheless, inhibition of the HOCl ? COX - TXA2 pathway unmasked the effects of additional MPO-derived radicals with a marked vasodilatorypotential in SMAs.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
vazokonstrikció
Megjelenés:Acta Physiologica. - 214 : 1 (2015), p. 109-123. -
További szerzők:Pető Attila (1990-) (általános orvos) Fülöp Gábor Áron (1988-) (általános orvos) Rutkai Ibolya (1985-) (molekuláris biológus) Pásztorné Tóth Enikő (1966-) (laboratóriumi analitikus) Fagyas Miklós (1984-) (orvos) Kalász Judit (1986-) (molekuláris biológus) Édes István (1952-) (kardiológus) Tóth Attila (1971-) (biológus) Papp Zoltán (1965-) (kardiológus, élettanász)
Pályázati támogatás:K 84300
OTKA
K 109083
OTKA
TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Kardiológia Kutatócsoport
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
Borító:

10.

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
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

11.

001-es BibID:BIBFORM072384
Első szerző:Csongrádi Alexandra (molekuláris biológus)
Cím:Optimized angiotensin-converting enzyme activity assay for the accurate diagnosis of sarcoidosis / Alexandra Csongrádi, Attila Enyedi, István Takács, Tamás Végh , Ivetta S. Mányiné, Zsófia Pólik, István Tibor Altorjay, József Balla, György Balla, István Édes, János Kappelmayer, Attila Tóth, Zoltán Papp, Miklós Fagyas
Dátum:2018
Megjegyzések:Background:Serum angiotensin-converting enzyme (ACE) activity determination can aid the early diagnosis of sarcoidosis. We aimed to optimize a fluorescent kinetic assay for ACE activity by screening the confounding effects of endogenous ACE inhibitors and interfering factors. Genotype-dependent and genotype-independent reference values of ACE activity were established, and their diagnostic accuracies were validated in a clinical study.Methods:Internally quenched fluorescent substrate, Abz-FRK(Dnp)P-OH was used for ACE-activity measurements. A total of 201 healthy individuals and 59 presumably sarcoidotic patients were enrolled into this study. ACE activity and insertion/deletion (I/D) genotype of the ACE gene were determined.Results:Here we report that serum samples should be diluted at least 35-fold to eliminate the endogenous inhibitor effect of albumin. No significant interferences were detected: up to a triglyceride concentration of 16 mM, a hemoglobin concentration of 0.71 g/L and a bilirubin concentration of 150 ?M. Genotype-dependent reference intervals were considered as 3.76?11.25 U/L, 5.22?11.59 U/L, 7.19?14.84 U/L for II, ID and DD genotypes, respectively. I/D genotype-independent reference interval was established as 4.85?13.79 U/L. An ACE activity value was considered positive for sarcoidosis when it exceeded the upper limit of the reference interval. The optimized assay with genotype-dependent reference ranges resulted in 42.5% sensitivity, 100% specificity, 100% positive predictive value and 32.4% negative predictive value in the clinical study, whereas the genotype-independent reference range proved to have inferior diagnostic efficiency.Conclusions:An optimized fluorescent kinetic assay of serum ACE activity combined with ACE I/D genotype determination is an alternative to invasive biopsy for confirming the diagnosis of sarcoidosis in a significant percentage of patients.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
ACE
angiotensin-converting enzyme
genotype
reference interval
sarcoidosis
Megjelenés:Clinical chemistry and laboratory medicine. - 56 : 7 (2018), p. 1117-1125. -
További szerzők:Enyedi Attila (1975-) (sebész) Takács István (1963-) (sebész) Végh Tamás (1975-) (aneszteziológus, intenzív terápiás szakorvos) Mányiné Siket Ivetta (1962-) (laborasszisztens) Pólik Zsófia Altorjay István (1991-) (orvos, kardiológus) Balla József (1959-) (belgyógyász, nephrológus) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Édes István (1952-) (kardiológus) Kappelmayer János (1960-) (laboratóriumi szakorvos) Tóth Attila (1971-) (biológus) Papp Zoltán (1965-) (kardiológus, élettanász) Fagyas Miklós (1984-) (orvos)
Pályázati támogatás:PD 116212
NKFIH
K 116940
OTKA
ÚNKP-17-4-I-DE-40
ÚNKP
GINOP-2.3.2-15-2016-00043
GINOP
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

12.

001-es BibID:BIBFORM052173
Első szerző:Czikora Ágnes (molekuláris biológus)
Cím:Structure-activity relationships of vanilloid receptor agonists for arteriolar TRPV1 / Á. Czikora, E. Lizanecz, P. Bakó, I. Rutkai, F. Ruzsnavszky, J. Magyar, R. Pórszász, T. Kark, A. Facskó, Z. Papp, I. Édes, A. Tóth
Dátum:2012
ISSN:0007-1188
Megjegyzések:Summary Background and purpose: The vanilloid receptor 1 (TRPV1) plays a role in the activation of sensory neurons by various painful stimuli and became a therapeutic target. However, functional TRPV1 expression was also observed in the peripheral arteries affecting microvascular diameter. Experimental approach: Sensory TRPV1 activation was measured by eye wiping tests. Arteriolar TRPV1 mediated smooth muscle specific responses (arteriolar diameter, changes in intracellular Ca2+) were determined in isolated, pressurized skeletal muscle arterioles (from the rat and wild type or TRPV1-/- mice, n = 130) or in isolated canine smooth muscle cells. Vascular pharmacology of TRPV1 agonists (potency, efficacy, kinetics of action and receptor desensitization) was determined in isolated skeletal muscle arteries of the rat. Key results: Capsaicin evoked a similar constriction as norepinephrine, which was absent in TRPV knockout mice and was competitively inhibited by a TRPV1 antagonist AMG9810. Capsaicin activation resulted in an increase in intracellular Ca2+ in the arteriolar wall as well as in isolated smooth muscle cells. Other TRPV1 agonists evoked similar vascular constrictions (MSK-195, JYL-79) or were without effect (resiniferatoxin, JYL-273), although all resulted in a sensory activation (eye wiping). Maximal dose of agonists gave different kinetics of arteriolar response. A complete desensitization (tachyphylaxis) of arteriolar TRPV1 was observed (with the exception of capsaicin). Application of the partial agonist JYL-1511 suggested that about 10% TRPV1 activation is sufficient to evoke vascular tachyphylaxis without sensory activation. Conclusions and implications: Our data suggests that arteriolar TRPV1 has different structure-activity relationship compared to sensory neuron located receptor in the rat.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
vanilloid receptor (TRPV1)
resistance artery
vascular autoregulation
Megjelenés:British Journal of Pharmacology. - 165 : 6 (2012), p. 1801-1812. -
További szerzők:Lizanecz Erzsébet (1978-) (orvos) Bakó P. Rutkai Ibolya (1985-) (molekuláris biológus) Ruzsnavszky Ferenc (1984-) (élettanász) Magyar János (1961-) (élettanász) Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus) Kark Tamás (1981-) (orvos) Facskó Andrea (1953-) (szemész) Papp Zoltán (1965-) (kardiológus, élettanász) Édes István (1952-) (kardiológus) Tóth Attila (1971-) (biológus)
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Vascularis rizikó- és stroke betegek vizsgálata
K68077
OTKA
K84300
OTKA
ETT 377/2009
Egyéb
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
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