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Human Tissue Angiotensin Converting Enzyme (ACE) Activity Is Regulated by Genetic Polymorphisms, Posttranslational Modifications, Endogenous Inhibitors and Secretion in the Serum, Lungs and Heart.
Bánhegyi, Viktor; Enyedi, Attila; Fülöp, Gábor Áron; Oláh, Attila; Siket, Ivetta Mányiné; Váradi, Csongor; Bottyán, Klaudia; Lódi, Mária; Csongrádi, Alexandra; Umar, Azeem J; Fagyas, Miklós; Czuriga, Dániel; Édes, István; Pólos, Miklós; Merkely, Béla; Csanádi, Zoltán; Papp, Zoltán; Szabó, Gábor; Radovits, Tamás; Takács, István; Tóth, Attila.
  • Bánhegyi V; Division of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.
  • Enyedi A; Doctoral School of Kálmán Laki, University of Debrecen, 4032 Debrecen, Hungary.
  • Fülöp GÁ; Department of Cardiac Surgery, University of Halle, 06120 Halle (Saale), Germany.
  • Oláh A; Division of Thoracic Surgery, Department of Surgery, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.
  • Siket IM; Division of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.
  • Váradi C; Doctoral School of Kálmán Laki, University of Debrecen, 4032 Debrecen, Hungary.
  • Bottyán K; Heart and Vascular Center, Semmelweis University, 1122 Budapest, Hungary.
  • Lódi M; Heart and Vascular Center, Semmelweis University, 1122 Budapest, Hungary.
  • Csongrádi A; Division of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.
  • Umar AJ; Division of Thoracic Surgery, Department of Surgery, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.
  • Fagyas M; Division of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.
  • Czuriga D; Division of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.
  • Édes I; Division of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.
  • Pólos M; Doctoral School of Kálmán Laki, University of Debrecen, 4032 Debrecen, Hungary.
  • Merkely B; Division of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.
  • Csanádi Z; Doctoral School of Kálmán Laki, University of Debrecen, 4032 Debrecen, Hungary.
  • Papp Z; Division of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.
  • Szabó G; Division of Cardiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.
  • Radovits T; Division of Cardiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.
  • Takács I; Division of Cardiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.
  • Tóth A; Heart and Vascular Center, Semmelweis University, 1122 Budapest, Hungary.
Cells ; 10(7)2021 07 06.
Article in English | MEDLINE | ID: covidwho-1302160
ABSTRACT

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.
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Full text: Available Collection: International databases Database: MEDLINE Main subject: Peptidyl-Dipeptidase A Type of study: Prognostic study Limits: Aged / Female / Humans / Male / Middle aged Language: English Year: 2021 Document Type: Article Affiliation country: Cells10071708

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Peptidyl-Dipeptidase A Type of study: Prognostic study Limits: Aged / Female / Humans / Male / Middle aged Language: English Year: 2021 Document Type: Article Affiliation country: Cells10071708