Effect of propofol on calcium homeostasis in hypoxia-reoxygenated neonatal rat cardiomyocytes

Hyun S. Kim, Woo Chul Chang, Ki Chul Hwang, In-Geol Choi, Wyun K. Park

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

Intracellular Ca2+ overload induced by hypoxia-reoxygenation alters Ca2+ homeostasis, which plays an important role in myocardial cell injury. Even though propofol is known as a radical scavenger with Ca2+ channel blocking properties, little is known about cardioprotective effect associated with Ca2+ homeostasis in cardiomyocytes. In the present study, we showed that propofol protects cardiomyocytes against hypoxia-reoxygenation injury. In propofol-treated cardiomyocytes, we observed a decrease in the expression of pro-apoptotic protein Bax, cytochrome c, caspase-3 activation and intracellular Ca2+ content. We also found that propofol treatment enhanced expression of anti-apoptotic protein Bcl-2 and activation of ERK concerned with survival. Propofol attenuated alterations of genes involving Ca2+-regulatory mechanism and significantly modulated abnormal changes of SERCA2a genes in hypoxia-reoxygenated neonatal cardiomyocytes. These results suggest that propofol modulates the expression of genes involved in Ca2+ homeostasis, thereby producing cardioprotective effects through a reduction in apoptotic cell death.

Original languageEnglish
Pages (from-to)139-145
Number of pages7
JournalEuropean Journal of Pharmacology
Volume594
Issue number1-3
DOIs
Publication statusPublished - 2008 Oct 10

Fingerprint

Propofol
Cardiac Myocytes
Homeostasis
Calcium
Apoptosis Regulatory Proteins
Wounds and Injuries
Caspase 3
Genes
Hypoxia
Cell Death
Gene Expression

Keywords

  • Ca homeostasis
  • Cardiomyocytes
  • Hypoxia-reoxygenation
  • Propofol

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Pharmacology

Cite this

Effect of propofol on calcium homeostasis in hypoxia-reoxygenated neonatal rat cardiomyocytes. / Kim, Hyun S.; Chang, Woo Chul; Hwang, Ki Chul; Choi, In-Geol; Park, Wyun K.

In: European Journal of Pharmacology, Vol. 594, No. 1-3, 10.10.2008, p. 139-145.

Research output: Contribution to journalArticle

Kim, Hyun S. ; Chang, Woo Chul ; Hwang, Ki Chul ; Choi, In-Geol ; Park, Wyun K. / Effect of propofol on calcium homeostasis in hypoxia-reoxygenated neonatal rat cardiomyocytes. In: European Journal of Pharmacology. 2008 ; Vol. 594, No. 1-3. pp. 139-145.
@article{ccdeaae3249641f89bc7a7d0e063cb08,
title = "Effect of propofol on calcium homeostasis in hypoxia-reoxygenated neonatal rat cardiomyocytes",
abstract = "Intracellular Ca2+ overload induced by hypoxia-reoxygenation alters Ca2+ homeostasis, which plays an important role in myocardial cell injury. Even though propofol is known as a radical scavenger with Ca2+ channel blocking properties, little is known about cardioprotective effect associated with Ca2+ homeostasis in cardiomyocytes. In the present study, we showed that propofol protects cardiomyocytes against hypoxia-reoxygenation injury. In propofol-treated cardiomyocytes, we observed a decrease in the expression of pro-apoptotic protein Bax, cytochrome c, caspase-3 activation and intracellular Ca2+ content. We also found that propofol treatment enhanced expression of anti-apoptotic protein Bcl-2 and activation of ERK concerned with survival. Propofol attenuated alterations of genes involving Ca2+-regulatory mechanism and significantly modulated abnormal changes of SERCA2a genes in hypoxia-reoxygenated neonatal cardiomyocytes. These results suggest that propofol modulates the expression of genes involved in Ca2+ homeostasis, thereby producing cardioprotective effects through a reduction in apoptotic cell death.",
keywords = "Ca homeostasis, Cardiomyocytes, Hypoxia-reoxygenation, Propofol",
author = "Kim, {Hyun S.} and Chang, {Woo Chul} and Hwang, {Ki Chul} and In-Geol Choi and Park, {Wyun K.}",
year = "2008",
month = "10",
day = "10",
doi = "10.1016/j.ejphar.2008.07.027",
language = "English",
volume = "594",
pages = "139--145",
journal = "European Journal of Pharmacology",
issn = "0014-2999",
publisher = "Elsevier",
number = "1-3",

}

TY - JOUR

T1 - Effect of propofol on calcium homeostasis in hypoxia-reoxygenated neonatal rat cardiomyocytes

AU - Kim, Hyun S.

AU - Chang, Woo Chul

AU - Hwang, Ki Chul

AU - Choi, In-Geol

AU - Park, Wyun K.

PY - 2008/10/10

Y1 - 2008/10/10

N2 - Intracellular Ca2+ overload induced by hypoxia-reoxygenation alters Ca2+ homeostasis, which plays an important role in myocardial cell injury. Even though propofol is known as a radical scavenger with Ca2+ channel blocking properties, little is known about cardioprotective effect associated with Ca2+ homeostasis in cardiomyocytes. In the present study, we showed that propofol protects cardiomyocytes against hypoxia-reoxygenation injury. In propofol-treated cardiomyocytes, we observed a decrease in the expression of pro-apoptotic protein Bax, cytochrome c, caspase-3 activation and intracellular Ca2+ content. We also found that propofol treatment enhanced expression of anti-apoptotic protein Bcl-2 and activation of ERK concerned with survival. Propofol attenuated alterations of genes involving Ca2+-regulatory mechanism and significantly modulated abnormal changes of SERCA2a genes in hypoxia-reoxygenated neonatal cardiomyocytes. These results suggest that propofol modulates the expression of genes involved in Ca2+ homeostasis, thereby producing cardioprotective effects through a reduction in apoptotic cell death.

AB - Intracellular Ca2+ overload induced by hypoxia-reoxygenation alters Ca2+ homeostasis, which plays an important role in myocardial cell injury. Even though propofol is known as a radical scavenger with Ca2+ channel blocking properties, little is known about cardioprotective effect associated with Ca2+ homeostasis in cardiomyocytes. In the present study, we showed that propofol protects cardiomyocytes against hypoxia-reoxygenation injury. In propofol-treated cardiomyocytes, we observed a decrease in the expression of pro-apoptotic protein Bax, cytochrome c, caspase-3 activation and intracellular Ca2+ content. We also found that propofol treatment enhanced expression of anti-apoptotic protein Bcl-2 and activation of ERK concerned with survival. Propofol attenuated alterations of genes involving Ca2+-regulatory mechanism and significantly modulated abnormal changes of SERCA2a genes in hypoxia-reoxygenated neonatal cardiomyocytes. These results suggest that propofol modulates the expression of genes involved in Ca2+ homeostasis, thereby producing cardioprotective effects through a reduction in apoptotic cell death.

KW - Ca homeostasis

KW - Cardiomyocytes

KW - Hypoxia-reoxygenation

KW - Propofol

UR - http://www.scopus.com/inward/record.url?scp=50549084164&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=50549084164&partnerID=8YFLogxK

U2 - 10.1016/j.ejphar.2008.07.027

DO - 10.1016/j.ejphar.2008.07.027

M3 - Article

C2 - 18674530

AN - SCOPUS:50549084164

VL - 594

SP - 139

EP - 145

JO - European Journal of Pharmacology

JF - European Journal of Pharmacology

SN - 0014-2999

IS - 1-3

ER -