open access

Vol 64, No 2 (2006)
Other
Published online: 2006-02-16
Submitted: 2012-12-28
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ORIGINAL ARTICLE
Regulation of eNOS expression in HCAEC cell line treated with opioids and proinflammatory cytokines

Monika Seidel, Hanna Billert, Maciej Kurpisz
Kardiol Pol 2006;64(2):153-158.

open access

Vol 64, No 2 (2006)
Other
Published online: 2006-02-16
Submitted: 2012-12-28

Abstract


Background: Nitric oxide (NO) generated by endothelial nitric oxide synthase (eNOS) plays a crucial role in vascular function and homeostasis. eNOS activity maintains normal vascular tone, regulates leukocyte-endothelial cell interactions, inhibits platelet aggregation, limits smooth muscle cell proliferation and influences cardiac myocyte contractility. The loss of endothelium-derived NO has been shown to result in serious cardiovascular abnormalities, which may indicate eNOS involvement in the origin/development of cardiovascular disorders.
Aim: Evaluation of eNOS mRNA level in the endothelium of human coronary arteries upon opioids treatment (mediators of ischaemic preconditioning) and after incubation with proinflammatory cytokines (stress stimuli). Methods: Different concentrations of β-endorphin, endomorphin-1 and endomorphin-2 (alone or in combination with the opioid receptor blocker naloxone) as well as different concentrations of cytokines alone (IL-1β, TNF-α) or in combination were applied to in vitro cultured human coronary artery endothelial cells (HCAEC). After 24 hrs incubation, the cells were harvested, mRNA extracted and relative quantification of eNOS mRNA was conducted using real-time PCR.
Results:
Opioid treatment altered eNOS expression; however, none of the changes reached a statistically significant level. As for proinflammatory cytokines, both TNF-α and IL-1β substantially down-regulated the eNOS mRNA level (p

Abstract


Background: Nitric oxide (NO) generated by endothelial nitric oxide synthase (eNOS) plays a crucial role in vascular function and homeostasis. eNOS activity maintains normal vascular tone, regulates leukocyte-endothelial cell interactions, inhibits platelet aggregation, limits smooth muscle cell proliferation and influences cardiac myocyte contractility. The loss of endothelium-derived NO has been shown to result in serious cardiovascular abnormalities, which may indicate eNOS involvement in the origin/development of cardiovascular disorders.
Aim: Evaluation of eNOS mRNA level in the endothelium of human coronary arteries upon opioids treatment (mediators of ischaemic preconditioning) and after incubation with proinflammatory cytokines (stress stimuli). Methods: Different concentrations of β-endorphin, endomorphin-1 and endomorphin-2 (alone or in combination with the opioid receptor blocker naloxone) as well as different concentrations of cytokines alone (IL-1β, TNF-α) or in combination were applied to in vitro cultured human coronary artery endothelial cells (HCAEC). After 24 hrs incubation, the cells were harvested, mRNA extracted and relative quantification of eNOS mRNA was conducted using real-time PCR.
Results:
Opioid treatment altered eNOS expression; however, none of the changes reached a statistically significant level. As for proinflammatory cytokines, both TNF-α and IL-1β substantially down-regulated the eNOS mRNA level (p
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Keywords

eNOS; opioids; proinflammatory cytokines; cardiovascular disease

About this article
Title

ORIGINAL ARTICLE
Regulation of eNOS expression in HCAEC cell line treated with opioids and proinflammatory cytokines

Journal

Kardiologia Polska (Polish Heart Journal)

Issue

Vol 64, No 2 (2006)

Pages

153-158

Published online

2006-02-16

Bibliographic record

Kardiol Pol 2006;64(2):153-158.

Keywords

eNOS
opioids
proinflammatory cytokines
cardiovascular disease

Authors

Monika Seidel
Hanna Billert
Maciej Kurpisz

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