Document Detail

Differential activation of protein kinase C between ischemic and pharmacological preconditioning in the rabbit heart.
MedLine Citation:
PMID:  14529578     Owner:  NLM     Status:  MEDLINE    
The objective of the present study was to investigate the differential activation of protein kinase C between ischemic (IPC) and pharmacological preconditioning (PPC) in the rabbit heart. Control, IPC, diazoxide (Diaz), and chelerythrine (Chel)+IPC groups underwent prolonged coronary artery occlusion (CAO) for 30 minutes followed by 180 minutes' reperfusion (protocol I). In protocol II, sham, IPC-only, Diaz-only, and Chel+IPC-only groups did not undergo prolonged CAO. IPC was induced with 4 cycles of 5-min regional ischemia and 10-min reperfusion before prolonged CAO. Diaz (5 mg/kg) was administered 30 min before prolonged CAO. Chel (5 mg/kg) was administered 5 min before the IPC procedure. Infarct size was determined by tetrazolium staining. Assessment of protein kinase C (PKC) isoforms from a left ventricular (LV) sample was conducted by western blotting. Apoptosis in situ was determined by TUNEL assay. The infarction area in the IPC (11.6 +/- 1.0%) and Diaz (19.5 +/- 3.8%) groups was reduced significantly (p< 0.01, p< 0.05) relative to the control group (40.0 +/- 3.8%). The reduction by IPC was abolished by pretreatment with Chel. Apoptosis was significantly decreased (p< 0.01) in the IPC and diazoxide groups compared with the control and Chel+IPC groups (control: 4.78 +/- 0.56% vs. IPC: 2.00 +/- 0.38% vs. Diaz: 2.20 +/- 0.32% vs. Chel+IPC: 4.32 +/- 0.41%) and DNA laddering was attenuated in the IPC and Diaz groups. Membrane PKC-epsilon levels in the IPC and Diaz groups increased significantly relative to the control and Chel+IPC groups. Membrane PKC-epsilon levels in the IPC-only group showed greater increases than the Diaz-only and Chel+IPC-only groups. These findings suggest that whereas PPC suppresses apoptosis when diazoxide opens mitochondrial K(ATP) channels and then activates PKC-epsilon through ischemia-reperfusion, IPC activates PKC-epsilon in the particulate fraction prior to continuous ischemia-reperfusion. We concluded that the difference between IPC and PPC appears to consist in the difference in the timing of PKC-epsilon activation, though both IPC and PPC provide the cardioprotection in ischemia-reperfusion injury.
Shinji Okubo; Yujirou Tanabe; Nakaba Fujioka; Kenji Takeda; Noboru Takekoshi
Related Documents :
8641008 - Role of activation of protein kinase c in the infarct size-limiting effect of ischemic ...
12061258 - Studies on the signal cascade mechanism mediating the cardioprotective actions of brady...
9386178 - Changes in myocardial electrical impedance induced by coronary artery occlusion in pigs...
15802488 - The role of beta-adrenergic receptor signaling in cardioprotection.
7977058 - Radionuclide assessment of right ventricular contractile reserve after acute myocardial...
8576778 - Multiple risk factors for coronary heart disease in patients with hypertension.
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  The Japanese journal of physiology     Volume:  53     ISSN:  0021-521X     ISO Abbreviation:  Jpn. J. Physiol.     Publication Date:  2003 Jun 
Date Detail:
Created Date:  2003-10-07     Completed Date:  2004-06-24     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  2985184R     Medline TA:  Jpn J Physiol     Country:  Japan    
Other Details:
Languages:  eng     Pagination:  173-80     Citation Subset:  IM    
Department of Cardiology, Kanazawa Medical University, 1-1 Daigaku, Uchinada, Kahoku, Ishikawa 920-0293, Japan.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Cardiotonic Agents / pharmacology
Conditioning (Psychology)*
DNA Fragmentation
Diazoxide / pharmacology*
Drug Synergism
Enzyme Activation
Enzyme Inhibitors / pharmacology*
Heart / drug effects*
Ischemic Preconditioning, Myocardial*
Isoenzymes / metabolism
Myocardial Infarction / pathology
Myocardium / enzymology
Myocytes, Cardiac
Phenanthridines / pharmacology*
Protein Kinase C / metabolism*
Ventricular Function, Left
Reg. No./Substance:
0/Alkaloids; 0/Benzophenanthridines; 0/Cardiotonic Agents; 0/Enzyme Inhibitors; 0/Isoenzymes; 0/Phenanthridines; 34316-15-9/chelerythrine; 364-98-7/Diazoxide; EC Kinase C

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  The gating and conductance properties of Cav3.2 low-voltage-activated T-type calcium channels.
Next Document:  Vascular endothelial growth factor, capillarization, and function of the rat plantaris muscle at the...