CCL

Összesen 3 találat.
#/oldal:
Részletezés:
Rendezés:

1.

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
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

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
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

3.

001-es BibID:BIBFORM074692
Első szerző:Bánhegyi Viktor (kardiológus)
Cím:A keringésbe szekretált angiotenzin konvertáló enzim (ACE) nem a tüdőből származik / Bánhegyi Viktor, Enyedi Attila, Váradi Csongor, Fagyas Miklós, MÁnyiné Siket Ivetta, Bottyán Klaudia, Tóth Attila, Takács István
Dátum:2018
Tárgyszavak:Orvostudományok Klinikai orvostudományok idézhető absztrakt
angiotenzin konvertáló enzim (ACE)
Megjelenés:Medicina Thoracalis. - 71 : 3 (2018), p. 154. -
További szerzők:Enyedi Attila (1975-) (sebész) Váradi Csongor (1984-) (sebész, mellkassebész szakorvos) Fagyas Miklós (1984-) (orvos) Mányiné Siket Ivetta (1962-) (laborasszisztens) Bottyán Klaudia Tóth Attila (kardiológus) Takács István (1963-) (sebész)
Pályázati támogatás:GINOP-2.3.2-15-2016-0004
GINOP
EFOP-3.6.2-16-2017-00006
EFOP
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Rekordok letöltése1