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001-es BibID:BIBFORM097205
035-os BibID:(cikkazonosító)11064 (scopus)85116968958 (wos)000716921300001
Első szerző:Bódi Beáta (molekuláris biológus)
Cím:Alterations in ACE and ACE2 Activities and Cardiomyocyte Signaling Underlie Improved Myocardial Function in a Rat Model of Repeated Remote Ischemic Conditioning / Beáta Bódi, Patrick M. Pilz, Lilla Mártha, Miriam Lang, Ouafa Hamza, Miklós Fagyas, Petra L. Szabó, Dietmar Abraham, Attila Tóth, Bruno K. Podesser, Attila Kiss, Zoltán Papp
Dátum:2021
ISSN:1661-6596 1422-0067
Megjegyzések:Post-ischemic left ventricular (LV) remodeling and its hypothetical prevention by repeated remote ischemic conditioning (rRIC) in male Sprague?Dawley rats were studied. Myocardial infarction (MI) was evoked by permanent ligation of the left anterior descending coronary artery (LAD), and myocardial characteristics were tested in the infarcted anterior and non-infarcted inferior LV re-gions four and/or six weeks later. rRIC was induced by three cycles of five-minute-long unilateral hind limb ischemia and five minutes of reperfusion on a daily basis for a period of two weeks starting four weeks after LAD occlusion. Sham operated animals served as controls. Echocardio-graphic examinations and invasive hemodynamic measurements revealed distinct changes in LV systolic function between four and six weeks after MI induction in the absence of rRIC (i.e., LV ejection fraction (LVEF) decreased from 52.8 ? 2.1% to 50 ? 1.6%, mean ? SEM, p < 0.05) and in the presence of rRIC (i.e., LVEF increased from 48.2 ? 4.8% to 55.2 ? 4.1%, p < 0.05). Angioten-sin-converting enzyme (ACE) activity was about five times higher in the anterior LV wall at six weeks than that in sham animals. Angiotensin-converting enzyme 2 (ACE2) activity roughly doubled in post-ischemic LVs. These increases in ACE and ACE2 activities were effectively miti-gated by rRIC. Ca2+-sensitivities of force production (pCa50) of LV permeabilized cardiomyocytes were increased at six weeks after MI induction together with hypophosphorylation of 1) cardiac troponin I (cTnI) in both LV regions, and 2) cardiac myosin-binding protein C (cMyBP-C) in the anterior wall. rRIC normalized pCa50, cTnI and cMyBP-C phosphorylations. Taken together, post-ischemic LV remodeling involves region-specific alterations in ACE and ACE2 activities to-gether with changes in cardiomyocyte myofilament protein phosphorylation and function. rRIC has the potential to prevent these alterations and to improve LV performance following MI.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
repeated remote ischemic conditioning
cardiomyocyte mechanics
signaling
Megjelenés:International Journal Of Molecular Sciences. - 22 : 20 (2021), p. 1-17. -
További szerzők:Pilz, Patrick M. Mártha Lilla Lang, Miriam Hamza, Ouafa Fagyas Miklós (1984-) (orvos) Szabó Petra L. Abraham, Dietmar Tóth Attila (1971-) (biológus) Podesser, Bruno Karl Kiss Attila Papp Zoltán (1965-) (kardiológus, élettanász)
Pályázati támogatás:GINOP-2.3.2-15-2016-00043
GINOP
Austria-Hungary Action Foundation: 92öu8
Egyéb
Ludwig Boltzmann Society: REM2017-20
Egyéb
2020-4.1.1-TKP2020
Egyéb
TKP2020-IKA-04
Egyéb
TKP2020-NKA04
Egyéb
FK 128809
OTKA
K 132623
OTKA
COST Action EU-CARDIOPROTECTION: CA16225
Egyéb
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM094562
035-os BibID:(cikkazonosító)24 (WoS)000639453800001 (Scopus)85104214308 (PubMed)33844095
Első szerző:Fülöp Gábor Áron (általános orvos)
Cím:Omecamtiv mecarbil evokes diastolic dysfunction and leads to periodic electromechanical alternans / Fülöp Gábor Á., Oláh Attila, Csipo Tamas, Kovács Árpád, Pórszász Róbert, Veress Roland, Horváth Balázs, Nagy László, Bódi Beáta, Fagyas Miklós, Helgadottir Solveig Lind, Bánhegyi Viktor, Juhász Béla, Bombicz Mariann, Priksz Daniel, Nanasi Peter, Merkely Béla, Édes István, Csanádi Zoltán, Papp Zoltán, Radovits Tamás, Tóth Attila
Dátum:2021
ISSN:0300-8428
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Basic Research In Cardiology. - 116 : 1 (2021), p. 24. -
További szerzők:Oláh Attila (sebész) Csípő Tamás (1990-) Kovács Árpád (1986-) (kardiológus) Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus) Veress Roland (1992-) (molekuláris biológus) Horváth Balázs (1981-) (élettanász) Nagy László (1988-) (orvos) Bódi Beáta (1989-) (molekuláris biológus) Fagyas Miklós (1984-) (orvos) Helgadottir, Solveig Lind Bánhegyi Viktor (1991-) (kardiológus) Juhász Béla (1978-) (kísérletes farmakológus) Bombicz Mariann (1987-) (gyógyszerész) Priksz Dániel (1989-) (farmakológus) Nánási Péter Pál ifj. (1987-) (sejtbiológus) Merkely Béla (1965-) (orvos) Édes István (1952-) (kardiológus) Csanádi Zoltán (1960-) (kardiológus) Papp Zoltán (1965-) (kardiológus, élettanász) Radovits Tamás Tóth Attila (1971-) (biológus)
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3.

001-es BibID:BIBFORM054413
Első szerző:Kalász Judit (molekuláris biológus)
Cím:Single acute stress-induced progesterone and ovariectomy alter cardiomyocyte contractile function in female rats / Judit Kalász, Enikő Pásztor Tóth, Beáta Bódi, Miklós Fagyas, Attila Tóth, Bhattoa Harjit Pal, Sándor G. Vári, Marta Balog, Senka Blažetić, Marija Heffer, Zoltán Papp, Attila Borbély
Dátum:2014
ISSN:0353-9504
Megjegyzések:AIM:To assess how ovarian-derived sex hormones (in particular progesterone) modify the effects of single acute stress on the mechanical and biochemical properties of left ventricular cardiomyocytes in the rat.METHODS:Non-ovariectomized (control, n=8) and ovariectomized (OVX, n=8) female rats were kept under normal conditions or were exposed to stress (control-S, n=8 and OVX-S, n=8). Serum progesterone levels were measured using a chemiluminescent immunoassay. Left ventricular myocardial samples were used for isometric force measurements and protein analysis. Ca(2+)-dependent active force (Factive), Ca(2+)-independent passive force (Fpassive), and Ca(2+)-sensitivity of force production were determined in single, mechanically isolated, permeabilized cardiomyocytes. Stress- and ovariectomy-induced alterations in myofilament proteins (myosin-binding protein C [MyBP-C], troponin I [TnI], and titin) were analyzed by sodium dodecyl sulfate gel electrophoresis using protein and phosphoprotein stainings.RESULTS:Serum progesterone levels were significantly increased in stressed rats (control-S, 35.6?4.8 ng/mL and OVX-S, 21.9?4.0 ng/mL) compared to control (10?2.9 ng/mL) and OVX (2.8?0.5 ng/mL) groups. Factive was higher in the OVX groups (OVX, 25.9?3.4 kN/m(2) and OVX-S, 26.3?3.0 kN/m(2)) than in control groups (control, 16.4?1.2 kN/m(2) and control-S, 14.4?0.9 kN/m(2)). Regarding the potential molecular mechanisms, Factive correlated with MyBP-C phosphorylation, while myofilament Ca(2+)-sensitivity inversely correlated with serum progesterone levels when the mean values were plotted for all animal groups. Fpassive was unaffected by any treatment.CONCLUSION:Stress increases ovary-independent synthesis and release of progesterone, which may regulate Ca(2+)-sensitivity of force production in left ventricular cardiomyocytes. Stress and female hormones differently alter Ca(2+)-dependent cardiomyocyte contractile force production, which may have pathophysiological importance during stress conditions affecting postmenopausal women.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
stress, progesteron, cardiomyocytes
Megjelenés:Croatian Medical Journal. - 55 : 3 (2014), p. 239-249. -
További szerzők:Pásztorné Tóth Enikő (1966-) (laboratóriumi analitikus) Bódi Beáta (1989-) (molekuláris biológus) Fagyas Miklós (1984-) (orvos) Tóth Attila (1971-) (biológus) Bhattoa Harjit Pal (1973-) (laboratóriumi szakorvos) Vári Sándor G. Balog Márta Blažetić, Senka Heffer, Marija Papp Zoltán (1965-) (kardiológus, élettanász) Borbély Attila (1978-) (kardiológus)
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4.

001-es BibID:BIBFORM064197
Első szerző:Kovács Árpád (kardiológus)
Cím:Renin overexpression leads to increased titin-based stiffness contributing to diastolic dysfunction in hypertensive mRen2 rats / Árpád Kovács, Gábor Á. Fülöp, Andrea Kovács, Tamás Csípő, Beáta Bódi, Dániel Priksz, Béla Juhász, Lívia Beke, Zoltán Hendrik, Gábor Méhes, Henk L. Granzier, István Édes, Miklós Fagyas, Zoltán Papp, Judit Barta, Attila Tóth
Dátum:2016
ISSN:0363-6135
Megjegyzések:Hypertension (HTN) is a major risk factor for heart failure. We investigated the influence of HTN on cardiac contraction and relaxation in transgenic renin overexpressing rats (carrying mouse Ren-2 renin gene, mRen2, n = 6). Blood pressure (BP) was measured. Cardiac contractility was characterized by echocardiography, cellular force measurements, and biochemical assays were applied to reveal molecular mechanisms. Sprague-Dawley (SD) rats (n = 6) were used as controls. Transgenic rats had higher circulating renin activity and lower cardiac angiotensin-converting enzyme two levels. Systolic BP was elevated in mRen2 rats (235.11 ? 5.32 vs. 127.03 ? 7.56 mmHg in SD, P < 0.05), resulting in increased left ventricular (LV) weight/body weight ratio (4.05 ? 0.09 vs. 2.77 ? 0.08 mg/g in SD, P < 0.05). Transgenic renin expression had no effect on the systolic parameters, such as LV ejection fraction, cardiomyocyte Ca(2+)-activated force, and Ca(2+) sensitivity of force production. In contrast, diastolic dysfunction was observed in mRen2 compared with SD rats: early and late LV diastolic filling ratio (E/A) was lower (1.14 ? 0.04 vs. 1.87 ? 0.08, P < 0.05), LV isovolumetric relaxation time was longer (43.85 ? 0.89 vs. 28.55 ? 1.33 ms, P < 0.05), cardiomyocyte passive tension was higher (1.74 ? 0.06 vs. 1.28 ? 0.18 kN/m(2), P < 0.05), and lung weight/body weight ratio was increased (6.47 ? 0.24 vs. 5.78 ? 0.19 mg/g, P < 0.05), as was left atrial weight/body weight ratio (0.21 ? 0.03 vs. 0.14 ? 0.03 mg/g, P < 0.05). Hyperphosphorylation of titin at Ser-12742 within the PEVK domain and a twofold overexpression of protein kinase C-? in mRen2 rats were detected. Our data suggest a link between the activation of renin-angiotensin-aldosterone system and increased titin-based stiffness through phosphorylation of titin's PEVK element, contributing to diastolic dysfunction.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
hypertension
passive stiffness
renin-angiotensin-aldosterone system
RAAS
diastolic dysfunction
titin phosphorylation
Megjelenés:American Journal Of Physiology-Heart And Circulatory Physiology. - 310 : 11 (2016), p. H1671-H1682. -
További szerzők:Fülöp Gábor Áron (1988-) (általános orvos) Kovács Andrea (1974-) (neurológus) Csípő Tamás (1990-) Bódi Beáta (1989-) (molekuláris biológus) Priksz Dániel (1989-) (farmakológus) Juhász Béla (1978-) (kísérletes farmakológus) Beke Lívia Hendrik Zoltán (1986-) (orvos) Méhes Gábor (1966-) (patológus) Granzier, Henk L. Édes István (1952-) (kardiológus) Fagyas Miklós (1984-) (orvos) Papp Zoltán (1965-) (kardiológus, élettanász) Barta Judit (1975-) (kardiológus) Tóth Attila (1971-) (biológus)
Pályázati támogatás:PD116212
OTKA
K109083
OTKA
K116940
OTKA
MEDIA
FP7
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
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5.

001-es BibID:BIBFORM088270
035-os BibID:(cikkazonosító)470 (WoS)000600100200006 (scopus)85097316669
Első szerző:Lódi Mária
Cím:Prophylactic, single-drug cardioprotection in a comparative, experimental study of doxorubicin-induced cardiomyopathy / Mária Lódi, Viktor Bánhegyi, Beáta Bódi, Alexandra Gyöngyösi, Árpád Kovács, Anita Árokszállási, Nazha Hamdani, Miklós Fagyas, István Édes, Zoltán Csanádi, István Czuriga, Zoltán Kisvárday, István Lekli, Péter Bai, Attila Tóth, Zoltán Papp, Dániel Czuriga
Dátum:2020
ISSN:1479-5876
Megjegyzések:BackgroundCardiomyopathy is a common side effect of doxorubicin (DOX) chemotherapy. Despite intensive research efforts in the field, there is still no evidence available for routine cardioprotective prophylaxis to prevent cardiotoxicity in the majority of oncological patients at low risk of cardiovascular disease. We have recently demonstrated the advantages of a prophylactic, combined heart failure therapy in an experimental model of DOX-induced cardiomyopathy. In the current work, we focus on individually applied prophylactic medications studied in the same translational environment to clarify their distinct roles in the prevention of DOX cardiotoxicity.MethodsTwelve-week-old male Wistar rats were divided into 5 subgroups. Prophylactic beta -blocker (BB, bisoprolol), angiotensin-converting enzyme inhibitor (ACEI, perindopril) or aldosterone antagonist (AA, eplerenone) treatments were applied 1 week before DOX administration, then 6 cycles of intravenous DOX chemotherapy were administered. Rats receiving only intravenous DOX or saline served as positive and negative controls. Blood pressure, heart rate, body weight, and echocardiographic parameters were monitored in vivo. Two months after the last DOX administration, the animals were sacrificed, and their heart and serum samples were frozen in liquid nitrogen for histological, mechanical, and biochemical measurements.ResultsAll prophylactic treatments increased the survival of DOX-receiving animals. The lowest mortality rates were seen in the BB and ACEI groups. The left ventricular ejection fraction was only preserved in the BB group. The DOX-induced increase in the isovolumetric relaxation time could not be prevented by any prophylactic treatment. A decreased number of apoptotic nuclei and a preserved myocardial ultrastructure were found in all groups receiving prophylactic cardioprotection, while the DOX-induced fibrotic remodelling and the increase in caspase-3 levels could only be substantially prevented by the BB and ACEI treatments.ConclusionPrimary prophylaxis with cardioprotective agents like BB or ACEI has a key role in the prevention of DOX-induced cardiotoxicity in healthy rats. Future human studies are necessary to implement this finding in the clinical management of oncological patients free of cardiovascular risk factors.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
doxorubicin
anthracycline
cardiotoxicity
animal model
heart failure
Megjelenés:Journal of Translational Medicine. - 18 : 1 (2020), p. 470. -
További szerzők:Bánhegyi Viktor (1991-) (kardiológus) Bódi Beáta (1989-) (molekuláris biológus) Gyöngyösi Alexandra (1990-) (táplálkozástudományi szakember) Kovács Árpád (1986-) (kardiológus) Árokszállási Anita (1982-) (orvos) Hamdani, Nazha Fagyas Miklós (1984-) (orvos) Édes István (1952-) (kardiológus) Csanádi Zoltán (1960-) (kardiológus) Czuriga István (1948-2018) (kardiológus) Kisvárday Zoltán (1957-) (biológus, neurobiológus) Lekli István (1981-) (gyógyszerész) Bai Péter (1976-) (biokémikus) Tóth Attila (1971-) (biológus) Papp Zoltán (1965-) (kardiológus, élettanász) Czuriga Dániel (1982-) (kardiológus)
Pályázati támogatás:GINOP-2.3.2-15-2016-00043
GINOP
EFOP-3.6.2-16-2017-00006
EFOP
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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