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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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Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM078999
035-os BibID:(cikkazonosító)P568
Első szerző:Bánhegyi Viktor (kardiológus)
Cím:Old dogma, new aspects : role of angiotensin converting enzymes in the cardiovascular continuum / V. Bánhegyi, M. Fagyas, I. Mányiné Siket, A. Enyedi, K. Bottyán, I. Édes, Z. Papp, A. Tóth
Dátum:2018
ISSN:0008-6363
Megjegyzések:The renin angiotensin aldosterone system (RAAS) plays a pivotal role in the cardiovascular pathophysiology and represents a starting point of cardiovascular diseases. Textbooks agree that the angiotensin converting enzyme (ACE) is produced in human endothelia related tissues. The goal of my work is to investigate this fact and the endothelia related enzymes (ACE, ACE2) in contrast of their endogenous regulation and secretion processes in a clinical based study. Lung tissue- and blood samples were collected from patients with lung surgery at the Department of Thoracic Surgery, University of Debrecen (n=71). We performed fluorescent based ACE, ACE2 activity measurements and ELISA experiments. In addition, we determined the ACE genotype and recorded the medical history. To the investigation of the ACE secretion mechanism, primary Human Aortic Endothelial Cells (HAOEC) was used under cell cultured circumstances. To measure the proper activity of tissue bound ACE2 we performed experiments with the special fluorescent substrate Abz-SPY (3-nitro). We found a significantly elevated ACE activity in the circulation respectively genotype groups ID (9.645 ± 0.4223 U/ml, n=36, p=0.0043) and DD (11.20 ± 0.6203 U/ml, n=26, p=0.0005) when compared to II (6.966 ± 0.5166 U/ml, n=9) group. Surprisingly, we did not find any genotype difference among the ACE activities in the lung tissue (ID: 3.034 ± 0.1996 U/ml, n=36, p=0.6421; DD: 2.709 ± 0.2495 U/ml, n=26, p=0.7920) when compared to the II (2.833 ± 0.3179 U/ml, n=9) patient group. Furthermore, signs for endogenous ACE inhibition were found. The direct administration of ACE specific substrate Abz-FRK (Dnp) to our HAOEC cell culture resulted 299.6 U/ml ACE activity which was inhibited over 90% via 200 nM Captopril. On the contrary, we cannot reveal any ACE2 specific activity in our cell culture system. Experiments with fluorescent substrate Abz-SPY (3-nitro) did not reveal any ACE2 signal in circulation in contrary at tissue related milieu we were able to measure ACE2 activity with high specificity. Our data suggests that the genotype dependent source of ACE significantly contributes to the circulating ACE, which is different from the lung. The endogenous inhibition of ACE conveys the idea that ACE activity is endogenously regulated in vivo. HAOEC cell culture provides an optimal model system for investigation of the mechanism of ACE secretion. Abz-SPY (3-nitro) is a specific fluorescent substrate for tissue related ACE2 activity measurement which can help us to understand how the ACE2 shed into the circulation. All in all, these results could help us in the understanding of how a cardiovascular disease starts and evolves.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idézhető absztrakt
Megjelenés:Cardiovascular Research. - 114 : Suppl1 (2018), p. S139. -
További szerzők:Fagyas Miklós (1984-) (orvos) Mányiné Siket Ivetta (1962-) (laborasszisztens) Enyedi Attila (1975-) (sebész) Bottyán Klaudia Édes István (1952-) (kardiológus) Papp Zoltán (1965-) (kardiológus, élettanász) Tóth Attila
Pályázati támogatás:GINOP-2.3.2-15-2016-00043
GINOP
OTKA 116940
OTKA
EFOP-3.6.2-16-2017-00006
EFOP
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Intézményi repozitóriumban (DEA) tárolt változat
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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)
Internet cím:elektronikus változat
DOI
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4.

001-es BibID:BIBFORM018438
Első szerző:Fehér Attila (orvos)
Cím:Caveolin-1 limits the contribution of BK(Ca) channel to EDHF-mediated arteriolar dilation: implications in diet-induced obesity / Feher, A., Rutkai, I., Beleznai, T., Ungvari, Z., Csiszar, A., Edes, I., Bagi, Z.
Dátum:2010
ISSN:0008-6363
Megjegyzések:Caveolin-1 (Cav-1) interacts with large conductance Ca(2+)-activated potassium channels (BKCa) and likely exerts a negative regulatory effect on the channel activity. We investigated the role of Cav-1 in modulating BK(Ca) channel-mediated, endothelium-derived hyperpolarizing factor (EDHF)-dependent arteriolar dilation in normal condition and in an experimental model of obesity. METHODS AND RESULTS: In isolated, pressurized (80 mmHg) gracilis muscle arterioles (approximately 100 microm) of Cav-1 knockout mice, acetylcholine (ACh)-induced, EDHF-mediated dilations were enhanced and were significantly reduced by the BK(Ca) channel inhibitor, iberiotoxin (IBTX), whereas IBTX had no effect on EDHF-mediated dilations in the wild-type mice. Dilations to the selective BK(Ca) channel opener, NS-1619 were augmented in the Cav-1 knockout mice. In high-fat diet-treated, obese rats ACh-induced coronary arteriolar dilations were preserved, whereas IBTX-sensitive, ACh-induced and also NS-1619-evoked vasodilations were augmented when compared with lean animals. In coronary arterioles of obese rats a reduced protein expression of Cav-1 was detected by western immunoblotting and immunohistochemistry. Moreover, in coronary arterioles of lean rats, disruption of caveolae with methyl-beta-cyclodextrin augmented IBTX-sensitive, ACh-induced, and also NS-1619-evoked dilations. CONCLUSION: Thus, under normal conditions, Cav-1 limits the contribution of the BK(Ca) channel to EDHF-mediated arteriolar dilation. In obesity, a reduced expression of Cav-1 leads to greater contribution of the BK(Ca) channel to EDHF-mediated response, which seems essential for maintained coronary dilation.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Coronary
Microcirculation
EDHF
MaxiK channel
Caveolae
Megjelenés:Cardiovascular Research. - 87 : 4 (2010), p. 732-739. -
További szerzők:Rutkai Ibolya (1985-) (molekuláris biológus) Beleznai Tímea (1981-) (orvos) Ungvári Zoltán Csiszár Anna Édes István (1952-) (kardiológus) Bagi Zsolt (1974-) (orvos)
Pályázati támogatás:0735540T
Egyéb
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Intézményi repozitóriumban (DEA) tárolt változat
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5.

001-es BibID:BIBFORM018436
Első szerző:Rutkai Ibolya (molekuláris biológus)
Cím:Activation of prostaglandin E2 EP1 receptor increases arteriolar tone and blood pressure in mice with type 2 diabetes / Rutkai, I., Feher, A., Erdei, N., Henrion, D., Papp, Z., Edes, I., Koller, A., Kaley, G., Bagi, Z.
Dátum:2009
ISSN:0008-6363
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
diabetes
hypertension
arteriole
prostanoid
EP receptor
Megjelenés:Cardiovascular Research. - 83 : 1 (2009), p. 148-154. -
További szerzők:Fehér Attila (1982-) (orvos) Erdei Nóra (1979-) (orvos) Henrion, Daniel Papp Zoltán (1965-) (kardiológus, élettanász) Édes István (1952-) (kardiológus) Koller Ákos Kaley Gábor Bagi Zsolt (1974-) (orvos)
Pályázati támogatás:449/2006
OTKA
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DOI
Intézményi repozitóriumban (DEA) tárolt változat
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