Antiischemic effects of SB203580 are mediated through the inhibition of p38α mitogen-activated protein kinase: Evidence from ectopic expression of an inhibition-resistant kinase

Jody L. Martin, Metin Avkiran, Roy A. Quinlan, Philip Cohen, Michael S. Marber

    Research output: Contribution to journalArticlepeer-review

    64 Citations (Scopus)

    Abstract

    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 α 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 p38α MAPK, injury was reduced significantly by SB203580 present during simulated ischemia. In contrast, SB203580 did not protect cells expressing the SB203580-resistant form of p38α MAPK. These observations suggest that SB203580-mediated protection depends on the inhibition of p38α MAPK.

    Original languageEnglish
    Pages (from-to)750-752
    Number of pages3
    JournalCirculation Research
    Volume89
    Issue number9
    DOIs
    Publication statusPublished - 26 Oct 2001

    Keywords

    • Isolated cells
    • p38 mitogen-activated protein kinase
    • Preconditioning
    • SB203580
    • Signaling

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