Abstract
Protein kinase C (PKC) has been suggested to mediate, at least in part, multiple processes in the pathophysiological sequelae of myocardial ischemia. The present study demonstrates that the epsilon, eta and iota isozymes of PKC are translocated to nuclei in response to brief intervals of global ischemia as well as reperfusion of ischemic rat myocardium. Concomitant with the translocation of PKC isozymes to nuclei during ischemia, increased PKC-mediated nuclear protein phosphorylation was observed. Taken together, the present results demonstrate that nuclear signaling mechanisms are activated during myocardial ischemia that include PKC translocation and PKC-mediated nuclear protein phosphorylation.
Publication types
-
Research Support, Non-U.S. Gov't
-
Research Support, U.S. Gov't, P.H.S.
MeSH terms
-
Animals
-
Biomarkers / analysis
-
Blotting, Western
-
Cell Fractionation
-
Cell Nucleus / enzymology
-
Cell Nucleus / metabolism*
-
Cytosol / metabolism
-
Indoles / pharmacology
-
Isoenzymes / metabolism*
-
Male
-
Maleimides / pharmacology
-
Myocardial Ischemia / enzymology
-
Myocardial Ischemia / metabolism*
-
Myocardial Reperfusion
-
Myocardium / enzymology
-
Myocardium / metabolism*
-
Nuclear Proteins / metabolism*
-
Phosphorylation
-
Protein Kinase C / antagonists & inhibitors
-
Protein Kinase C / metabolism*
-
Protein Kinase C-epsilon
-
Rats
-
Rats, Sprague-Dawley
Substances
-
Biomarkers
-
Indoles
-
Isoenzymes
-
Maleimides
-
Nuclear Proteins
-
Prkce protein, rat
-
protein kinase C eta
-
Protein Kinase C
-
Protein Kinase C-epsilon
-
protein kinase C lambda
-
bisindolylmaleimide