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Effects of propofol on the expression of matric metalloproteinases in rat cardiac fibroblasts after hypoxia and reoxygenation.

Authors
 J. H. Jun  ;  J. E. Cho  ;  Y. H. Shim  ;  J. K. Shim  ;  Y. L. Kwak 
Citation
 BRITISH JOURNAL OF ANAESTHESIA, Vol.106(5) : 650-658, 2011 
Journal Title
BRITISH JOURNAL OF ANAESTHESIA
ISSN
 0007-0912 
Issue Date
2011
MeSH
Anesthetics, Intravenous/pharmacology* ; Animals ; Cardiotonic Agents/pharmacology ; Cell Hypoxia*/physiology ; Cell Movement/drug effects ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Cells, Cultured ; Extracellular Signal-Regulated MAP Kinases/drug effects ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Fibroblasts/drug effects ; Fibroblasts/enzymology ; Gene Expression Regulation, Enzymologic/drug effects ; Matrix Metalloproteinases/biosynthesis ; Matrix Metalloproteinases/drug effects* ; Matrix Metalloproteinases/genetics ; Myocardial Reperfusion Injury/enzymology* ; Myocardial Reperfusion Injury/pathology ; Propofol/pharmacology* ; Proto-Oncogene Proteins c-akt/drug effects ; Proto-Oncogene Proteins c-akt/metabolism ; RNA, Messenger/genetics ; Rats ; Rats, Sprague-Dawley ; Signal Transduction/drug effects ; Tissue Inhibitor of Metalloproteinases/biosynthesis ; Tissue Inhibitor of Metalloproteinases/drug effects ; Tissue Inhibitor of Metalloproteinases/genetics
Keywords
ischaemia/reperfusion ; matrix metalloproteinases ; propofol
Abstract
BACKGROUND: Propofol is known to protect the myocardium against ischaemia/reperfusion (I/R) injury through its antioxidant and anti-inflammatory properties. Matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) are involved in cell migration and invasion, and mediate tissue remodelling during I/R injury. They are regulated by various mechanisms including oxidative stress and AKT and ERK pathways. We investigated whether propofol affected the expression of MMPs and subsequent cell migration and invasion and the signalling pathways involved in primary rat cardiac fibroblasts undergoing hypoxia and reoxygenation.

METHODS: The phosphorylation of ERK and AKT signalling pathways was examined by western blot analysis in rat primary cardiac fibroblasts after hypoxia and reoxygenation. mRNA expression of MMP and TIMPS was analysed by real-time PCR, and proteolytic activities of MMP-2 and -9 were assessed. The effects of propofol on migration, invasion, wound healing, and cell proliferation activity were evaluated after reoxygenation.

RESULTS: Propofol induced AKT and ERK1/2 activation. Subsequent activation of MMPs resulted in increased cell migration, invasion, and wound-healing activity under hypoxia-reoxygenation, which was decreased by LY294002 (AKT inhibitor) and U0126 (ERK inhibitor) in rat cardiac fibroblasts. However, propofol had no effect on proliferation or viability of cardiac fibroblasts after hypoxia-reoxygenation.

CONCLUSIONS: Propofol affected the expression of MMPs and TIMPs and subsequently induced cell migration and invasive ability, through activation of the ERK and AKT signalling pathway in hypoxia-reoxygenated rat cardiac fibroblasts
Files in This Item:
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DOI
10.1093/bja/aer006
Appears in Collections:
1. College of Medicine (의과대학) > Research Institute (부설연구소) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Anesthesiology and Pain Medicine (마취통증의학교실) > 1. Journal Papers
Yonsei Authors
Kwak, Young Lan(곽영란) ORCID logo https://orcid.org/0000-0002-2984-9927
Shim, Yon Hee(심연희) ORCID logo https://orcid.org/0000-0003-1921-3391
Shim, Jae Kwang(심재광) ORCID logo https://orcid.org/0000-0001-9093-9692
Jun, Ji Hae(전지혜) ORCID logo https://orcid.org/0000-0002-8080-0715
Cho, Jang Eun(조장은)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/93034
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