Circulation Research. 2001
Published online before print October 4, 2001, doi: 10.1161/hh2101.099504
Published online before print October 4, 2001, doi: 10.1161/hh2101.099504
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Submitted on July 20, 2001
Revised on September 21, 2001
Accepted on September 21, 2001
Antiischemic Effects of SB203580 Are Mediated Through the Inhibition of p38
Mitogen-Activated Protein Kinase. Evidence From Ectopic Expression of an Inhibition-Resistant Kinase
From the Department of Cardiology (J.L.M., M.A., M.S.M.), King's College London, The Rayne Institute, St Thomas' Hospital, London; the Department of Biological Sciences (R.A.Q.), University of Durham; and the MRC Protein Phosphorylation Unit (P.C.), Department of Biochemistry, University of Dundee, UK.
* To whom correspondence should be addressed. E-mail: mike.marber{at}kcl.ac.uk.
The aim of the present study was to determine whether the attenuation of myocardial ischemic injury by SB203580 is due to the inhibition of p38 mitogen-activated protein kinase (MAPK) or to other documented nonspecific effects of the drug. We made adenoviral vectors encoding the isoform of p38 MAPK with or without site-directed mutations to prevent SB203580 binding and inhibition. In embryonal rat heart--derived cells and adult rat cardiocytes expressing wild-type p38 MAPK, injury was reduced significantly by SB203580 present during simulated ischemia. In contrast, SB203580 did not protect cells expressing the SB203580-resistant form of p38 MAPK. These observations suggest that SB203580-mediated protection depends on the inhibition of p38 MAPK.
Key words: SB203580 • p38 mitogen-activated protein kinase • preconditioning • isolated cells • signaling
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