Endothelin-converting enzyme-1 mRNA expression in human cardiovascular disease

Holger Bohnemeier, Yigal M. Pinto, F. Horkay, Miklós Tóth, A. Juhász-Nagy, Hans Dieter Orzechowski, Martin Paul

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Endothelin-converting enzyme-1 (ECE-1) plays a substantial role in activation of the endothelin (ET) system by cleaving the precursor, big ET-1, to the active peptide ET-1. The aim of this study was to investigate whether ECE-1 mRNA expression is modified in human cardiovascular disease. ECE-1 expression was related to echocardiographic data, drug treatment, age, sex, and NYHA heart failure classification. A quantitative PCR assay (qPCR) was established to measure ECE-1 mRNA in these samples. The ECE-1 measurements were normalized over a simultaneously performed GAPDH qPCR. The results indicate a higher ECE-1 expression level in atrial tissue samples of patients who have experienced a myocardial infarction compared with those who did not (ECE-1/GAPDH: 5.81 ± 0.76 fg/ng; n = 21 vs. 3.20 ± 0.51 fg/ng; n = 22; p = 0.007). The transverse diameter of the left atrium over 37 mm was associated with a lower ECE-1 expression (ECE-1/GAPDH: 3.11 ± 0.69 fg/ng; n = 18 vs. 5.12 ± 0.65 fg/ng; n = 25; p = 0.044). In assessing the drug treatment, decreased ECE-1 expression could be observed in patients who received a β-blocker (ECE-1/GAPDH: 3.90 ± 58 fg/ng; n = 31 vs. 5.81 ± 0.76 fg/ng; n = 12; p = 0.077). These data suggest an involvement of the ET system in cardiovascular disease that may be clinically important.

Original languageEnglish
JournalJournal of Cardiovascular Pharmacology
Volume31
Issue numberSUPPL. 1
Publication statusPublished - 1998

Fingerprint

Cardiovascular Diseases
Messenger RNA
Endothelins
Endothelin-1
Endothelin-Converting Enzymes
Polymerase Chain Reaction
Heart Atria
Pharmaceutical Preparations
Heart Failure
Myocardial Infarction
Peptides
Therapeutics

Keywords

  • Cardiovascular
  • Endothelin-converting enzyme
  • Human
  • mRNA expression
  • qPCR

ASJC Scopus subject areas

  • Pharmacology
  • Cardiology and Cardiovascular Medicine

Cite this

Bohnemeier, H., Pinto, Y. M., Horkay, F., Tóth, M., Juhász-Nagy, A., Orzechowski, H. D., & Paul, M. (1998). Endothelin-converting enzyme-1 mRNA expression in human cardiovascular disease. Journal of Cardiovascular Pharmacology, 31(SUPPL. 1).

Endothelin-converting enzyme-1 mRNA expression in human cardiovascular disease. / Bohnemeier, Holger; Pinto, Yigal M.; Horkay, F.; Tóth, Miklós; Juhász-Nagy, A.; Orzechowski, Hans Dieter; Paul, Martin.

In: Journal of Cardiovascular Pharmacology, Vol. 31, No. SUPPL. 1, 1998.

Research output: Contribution to journalArticle

Bohnemeier, H, Pinto, YM, Horkay, F, Tóth, M, Juhász-Nagy, A, Orzechowski, HD & Paul, M 1998, 'Endothelin-converting enzyme-1 mRNA expression in human cardiovascular disease', Journal of Cardiovascular Pharmacology, vol. 31, no. SUPPL. 1.
Bohnemeier, Holger ; Pinto, Yigal M. ; Horkay, F. ; Tóth, Miklós ; Juhász-Nagy, A. ; Orzechowski, Hans Dieter ; Paul, Martin. / Endothelin-converting enzyme-1 mRNA expression in human cardiovascular disease. In: Journal of Cardiovascular Pharmacology. 1998 ; Vol. 31, No. SUPPL. 1.
@article{ba90ce9ee94d4de5a7bc2743cbac0eb6,
title = "Endothelin-converting enzyme-1 mRNA expression in human cardiovascular disease",
abstract = "Endothelin-converting enzyme-1 (ECE-1) plays a substantial role in activation of the endothelin (ET) system by cleaving the precursor, big ET-1, to the active peptide ET-1. The aim of this study was to investigate whether ECE-1 mRNA expression is modified in human cardiovascular disease. ECE-1 expression was related to echocardiographic data, drug treatment, age, sex, and NYHA heart failure classification. A quantitative PCR assay (qPCR) was established to measure ECE-1 mRNA in these samples. The ECE-1 measurements were normalized over a simultaneously performed GAPDH qPCR. The results indicate a higher ECE-1 expression level in atrial tissue samples of patients who have experienced a myocardial infarction compared with those who did not (ECE-1/GAPDH: 5.81 ± 0.76 fg/ng; n = 21 vs. 3.20 ± 0.51 fg/ng; n = 22; p = 0.007). The transverse diameter of the left atrium over 37 mm was associated with a lower ECE-1 expression (ECE-1/GAPDH: 3.11 ± 0.69 fg/ng; n = 18 vs. 5.12 ± 0.65 fg/ng; n = 25; p = 0.044). In assessing the drug treatment, decreased ECE-1 expression could be observed in patients who received a β-blocker (ECE-1/GAPDH: 3.90 ± 58 fg/ng; n = 31 vs. 5.81 ± 0.76 fg/ng; n = 12; p = 0.077). These data suggest an involvement of the ET system in cardiovascular disease that may be clinically important.",
keywords = "Cardiovascular, Endothelin-converting enzyme, Human, mRNA expression, qPCR",
author = "Holger Bohnemeier and Pinto, {Yigal M.} and F. Horkay and Mikl{\'o}s T{\'o}th and A. Juh{\'a}sz-Nagy and Orzechowski, {Hans Dieter} and Martin Paul",
year = "1998",
language = "English",
volume = "31",
journal = "Journal of Cardiovascular Pharmacology",
issn = "0160-2446",
publisher = "Lippincott Williams and Wilkins",
number = "SUPPL. 1",

}

TY - JOUR

T1 - Endothelin-converting enzyme-1 mRNA expression in human cardiovascular disease

AU - Bohnemeier, Holger

AU - Pinto, Yigal M.

AU - Horkay, F.

AU - Tóth, Miklós

AU - Juhász-Nagy, A.

AU - Orzechowski, Hans Dieter

AU - Paul, Martin

PY - 1998

Y1 - 1998

N2 - Endothelin-converting enzyme-1 (ECE-1) plays a substantial role in activation of the endothelin (ET) system by cleaving the precursor, big ET-1, to the active peptide ET-1. The aim of this study was to investigate whether ECE-1 mRNA expression is modified in human cardiovascular disease. ECE-1 expression was related to echocardiographic data, drug treatment, age, sex, and NYHA heart failure classification. A quantitative PCR assay (qPCR) was established to measure ECE-1 mRNA in these samples. The ECE-1 measurements were normalized over a simultaneously performed GAPDH qPCR. The results indicate a higher ECE-1 expression level in atrial tissue samples of patients who have experienced a myocardial infarction compared with those who did not (ECE-1/GAPDH: 5.81 ± 0.76 fg/ng; n = 21 vs. 3.20 ± 0.51 fg/ng; n = 22; p = 0.007). The transverse diameter of the left atrium over 37 mm was associated with a lower ECE-1 expression (ECE-1/GAPDH: 3.11 ± 0.69 fg/ng; n = 18 vs. 5.12 ± 0.65 fg/ng; n = 25; p = 0.044). In assessing the drug treatment, decreased ECE-1 expression could be observed in patients who received a β-blocker (ECE-1/GAPDH: 3.90 ± 58 fg/ng; n = 31 vs. 5.81 ± 0.76 fg/ng; n = 12; p = 0.077). These data suggest an involvement of the ET system in cardiovascular disease that may be clinically important.

AB - Endothelin-converting enzyme-1 (ECE-1) plays a substantial role in activation of the endothelin (ET) system by cleaving the precursor, big ET-1, to the active peptide ET-1. The aim of this study was to investigate whether ECE-1 mRNA expression is modified in human cardiovascular disease. ECE-1 expression was related to echocardiographic data, drug treatment, age, sex, and NYHA heart failure classification. A quantitative PCR assay (qPCR) was established to measure ECE-1 mRNA in these samples. The ECE-1 measurements were normalized over a simultaneously performed GAPDH qPCR. The results indicate a higher ECE-1 expression level in atrial tissue samples of patients who have experienced a myocardial infarction compared with those who did not (ECE-1/GAPDH: 5.81 ± 0.76 fg/ng; n = 21 vs. 3.20 ± 0.51 fg/ng; n = 22; p = 0.007). The transverse diameter of the left atrium over 37 mm was associated with a lower ECE-1 expression (ECE-1/GAPDH: 3.11 ± 0.69 fg/ng; n = 18 vs. 5.12 ± 0.65 fg/ng; n = 25; p = 0.044). In assessing the drug treatment, decreased ECE-1 expression could be observed in patients who received a β-blocker (ECE-1/GAPDH: 3.90 ± 58 fg/ng; n = 31 vs. 5.81 ± 0.76 fg/ng; n = 12; p = 0.077). These data suggest an involvement of the ET system in cardiovascular disease that may be clinically important.

KW - Cardiovascular

KW - Endothelin-converting enzyme

KW - Human

KW - mRNA expression

KW - qPCR

UR - http://www.scopus.com/inward/record.url?scp=0031637641&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031637641&partnerID=8YFLogxK

M3 - Article

VL - 31

JO - Journal of Cardiovascular Pharmacology

JF - Journal of Cardiovascular Pharmacology

SN - 0160-2446

IS - SUPPL. 1

ER -