Találati lista | Tudóstér

001-es BibID:	BIBFORM098750
035-os BibID:	(cikkazonosító)1776
Első szerző:	Bódi Beáta (molekuláris biológus)
Cím:	Long-Term PDE-5A Inhibition Improves Myofilament Function in Left and Right Ventricular Cardiomyocytes through Partially Different Mechanisms in Diabetic Rat Hearts / Bódi Beáta, Kovács Árpád, Gulyás Hajnalka, Mártha Lilla, Tóth Attila, Mátyás Csaba, Barta Bálint András, Oláh Attila, Merkely Béla, Radovits Tamás, Papp Zoltán
Dátum:	2021
ISSN:	2076-3921
Megjegyzések:	Heart failure with preserved ejection fraction (HFpEF) and right ventricular (RV) dysfunction are frequent complications of diabetic cardiomyopathy. Here we aimed to characterize RV and left ventricular (LV) remodeling and its prevention by vardenafil (a long-acting phosphodiesterase5A (PDE-5A) inhibitor) administration in a diabetic HFpEF model. Zucker Diabetic Fatty (ZDF) and control, ZDF Lean (Lean) male rats received 10 mg/kg vardenafil (ZDF + Vard; Lean + Vard) per os, on a daily basis for a period of 25 weeks. In vitro force measurements, biochemical and histochemical assays were employed to assess cardiomyocyte function and signaling. Vardenafil treatment increased cyclic guanosine monophosphate (cGMP) levels and decreased 3-nitrotyrosine (3-NT) levels in the left and right ventricles of ZDF animals, but not in Lean animals. Cardiomyocyte passive tension (Fpassive) was higher in LV and RV cardiomyocytes of ZDF rats than in those receiving preventive vardenafil treatment. Levels of overall titin phosphorylation did not differ in the four experimental groups. Maximal Ca2+-activated force (Fmax) of LV and RV cardiomyocytes were preserved in ZDF animals. Ca2+-sensitivity of isometric force production (pCa50) was significantly higher in LV (but not in RV) cardiomyocytes of ZDF rats than in their counterparts in the Lean or Lean + Vard groups. In accordance, the phosphorylation levels of cardiac troponin I (cTnI) and myosin binding protein-C (cMyBP-C) were lower in LV (but not in RV) cardiomyocytes of ZDF animals than in their counterparts of the Lean or Lean + Vard groups. Vardenafil treatment normalized pCa50 values in LV cardiomyocytes, and it decreased pCa50 below control levels in RV cardiomyocytes in the ZDF + Vard group. Our data illustrate partially overlapping myofilament protein alterations for LV and RV cardiomyocytes in diabetic rat hearts upon long-term PDE-5A inhibition. While uniform patterns in cGMP, 3-NT and Fpassive levels predict identical effects of vardenafil therapy for the diastolic function in both ventricles, the uneven cTnI, cMyBP-C phosphorylation levels and pCa50 values implicate different responses for the systolic function.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk right ventricle HFpEF diabetic cardiomyopathy cardiomyocyte passive tension Ca2+ - sensitivity of force production myofilament protein phosphorylation vardenafil phosphodiesterase-5A
Megjelenés:	Antioxidants. - 10 : 11 (2021), p. 1-13. -
További szerzők:	Kovács Árpád (1986-) (kardiológus) Gulyás Hajnalka Mártha Lilla Tóth Attila (1971-) (biológus) Mátyás Csaba Barta Bálint András Oláh Attila Merkely Béla (1965-) (orvos) Radovits Tamás Papp Zoltán (1965-) (kardiológus, élettanász)
Pályázati támogatás:	GINOP-2.3.2-15-2016-00043 GINOP TKP2020-IKA-04 Egyéb TKP2020-NKA-04 Egyéb 2020-4.1.1-TKP2020 Egyéb NVKP_16-1-2016-0017 Egyéb
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon:

001-es BibID:	BIBFORM101728
035-os BibID:	(cikkazonosító)1465 (scopus)85123579850 (wos)000756238000001
Első szerző:	Csípő Tamás
Cím:	A Central Role for TRPM4 in Ca2+-Signal Amplification and Vasoconstriction / Csípő Tamás, Czikora Ágnes, Fülöp Gábor Á., Gulyás Hajnalka, Rutkai Ibolya, Tóth Enikő Pásztorné, Pórszász Róbert, Szalai Andrea, Bölcskei Kata, Helyes Zsuzsanna, Pintér Erika, Papp Zoltán, Ungvári Zoltán, Tóth Attila
Dátum:	2022
ISSN:	1661-6596 1422-0067
Megjegyzések:	Transient receptor potential melastatin-4 (TRPM4) is activated by an increase in intracellular Ca2+ concentration and is expressed on smooth muscle cells (SMCs). It is implicated in the myogenic constriction of cerebral arteries. We hypothesized that TRPM4 has a general role in intracellular Ca2+ signal amplification in a wide range of blood vessels. TRPM4 function was tested with the TRPM4 antagonist 9-phenanthrol and the TRPM4 activator A23187 on the cardiovascular responses of the rat, in vivo and in isolated basilar, mesenteric, and skeletal muscle arteries. TRPM4 inhibition by 9-phenanthrol resulted in hypotension and a decreased heart rate in the rat. TRPM4 inhibition completely antagonized myogenic tone development and norepinephrine-evoked vasoconstriction, and depolarization (high extracellular KCl concentration) evoked vasoconstriction in a wide range of peripheral arteries. Vasorelaxation caused by TRPM4 inhibition was accompanied by a significant decrease in intracellular Ca2+ concentration, suggesting an inhibition of Ca2+ signal amplification. Immunohistochemistry confirmed TRPM4 expression in the smooth muscle cells of the peripheral arteries. Finally, TRPM4 activation by the Ca2+ ionophore A23187 was competitively inhibited by 9-phenanthrol. In summary, TRPM4 was identified as an essential Ca2+-amplifying channel in peripheral arteries, contributing to both myogenic tone and agonist responses. These results suggest an important role for TRPM4 in the circulation. The modulation of TRPM4 activity may be a therapeutic target for hypertension. Furthermore, the Ca2+ ionophore A23187 was identified as the first high-affinity (nanomolar) direct activator of TRPM4, acting on the 9-phenanthrol binding site
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Ca2+ signaling vascular smooth muscle blood pressure regulation transient receptor potential melastatin-4 transient receptor potential
Megjelenés:	International Journal Of Molecular Sciences. - 23 : 3 (2022), p. 1-13. -
További szerzők:	Czikora Ágnes (1982-) (molekuláris biológus) Fülöp Gábor Áron (1988-) (általános orvos) Gulyás Hajnalka Rutkai Ibolya (1985-) (molekuláris biológus) Pásztorné Tóth Enikő (1966-) (laboratóriumi analitikus) Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus) Szalai Andrea (1968-) (analitikus) Bölcskei Kata Helyes Zsuzsanna Pintér Erika Papp Zoltán (1965-) (kardiológus, élettanász) Ungvári Zoltán Tóth Attila (1971-) (biológus)
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon:

001-es BibID:	BIBFORM090205
035-os BibID:	(WOS)000608951800001 (Scopus)85099552143
Első szerző:	Fagyas Miklós (orvos)
Cím:	Level of the SARS-CoV-2 receptor ACE2 activity is highly elevated in old-aged patients with aortic stenosis : implications for ACE2 as a biomarker for the severity of COVID-19 / Fagyas Miklós, Kertész Attila, Mányiné Siket Ivetta, Bánhegyi Viktor, Kracskó Bertalan, Szegedi Andrea, Szokol Miklós, Vajda Gusztáv, Rácz Ildikó, Gulyás Hajnalka, Szkibák Noémi, Rácz Vivien, Csanádi Zoltán, Papp Zoltán, Tóth Attila, Sipka Sándor
Dátum:	2021
ISSN:	2509-2715 2509-2723
Megjegyzések:	Coronavirus disease 2019 (COVID-19) has a high mortality in elderly patients with preexisting cardiovascular diseases. The cellular receptor of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the angiotensin converting enzyme 2 (ACE2), thereby implicating a link between cardiovascular diseases and SARS-CoV-2 susceptibility. Aortic stenosis (AS) represents a chronic inflammatory state with severe cardiovascular complications in the elderly, a prime condition for COVID-19 mortality. The circulating ACE2 levels were measured in 111 patients with severe AS and compared to patients with hypertension and healthy individuals. About 4-times higher circulating ACE2 activity was found in patients with severe AS than in hypertensives or healthy individuals (88.3?61.6., n=111, 20.6?13.4, n=540 and 16.1?7.4 mU/L, n=46, respectively). Patients with severe AS were older than patients with hypertension (80?6 years vs. 60?15 years, P<0.05). Serum ACE2 activity correlated negatively with the left ventricular ejection fraction, aortic root area, TAPSE and positively with the right ventricular systolic pressure, cardiac diameters in patients with AS. In contrast, circulating ACE2 activity was independent of the blood pressure, peak flow velocity at the aortic root, kidney function (GFR) and inflammatory state (CRP). We found no effect of RAAS inhibitory drugs on the serum ACE2 activity in this group of patients. Our results illustrate circulating ACE2 as a potential interface between chronic inflammation, cardiovascular disease and COVID-19 susceptibility. Elderly patients with AS have markedly elevated ACE2 levels together with altered left and right ventricular functions, which may pose higher risks during COVID-19. Our clinical data do not support a role for RAAS inhibitors in regulating circulating ACE2 levels. taa, km
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk ACE2 TAVI COVID-19 aortic stenosis age
Megjelenés:	GeroScience. - 43 : 1 (2021), p. 19-29. -
További szerzők:	Kertész Attila Béla (1973-) (kardiológus) Mányiné Siket Ivetta (1962-) (laborasszisztens) Bánhegyi Viktor (1991-) (kardiológus) Kracskó Bertalan (1986-) (orvos) Szegedi Andrea (kardiológus) Szokol Miklós (1971-) (kardiológus) Vajda Gusztáv (1956-) (kardiológus) Rácz Ildikó (1973-) (kardiológus) Gulyás Hajnalka Szkibák Noémi Rácz Vivien Csanádi Zoltán (1960-) (kardiológus) Papp Zoltán (1965-) (kardiológus, élettanász) Tóth Attila (1971-) (biológus) Sipka Sándor ifj. (1980-) (orvos)
Pályázati támogatás:	GINOP-2.3.2-15-2016-00043 GINOP EFOP-3.6.2-16-2017-00006 EFOP GINOP-2.3.2-15-2016-00050 GINOP OTKA-116940 OTKA NKFIH-K132623 Egyéb NKFIH-FK128809 Egyéb ED_18-1-2019-0028 Egyéb
Internet cím:	DOI Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon: