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knockout mouse
hearts
1 Cardiology Section, Veterans Affairs Medical Center, San Francisco, 94121; 2 Department of Molecular Pharmacology, Stanford University, Stanford 94305; 3 Ernest Gallo Clinic and Research Center, University of California, San Francisco 94608; and 4 Immunology Division, Department of Medicine, University of California, San Francisco, San Francisco, California 94143
Sphingosine-1-phosphate (S1P)
protects neonatal rat cardiac myocytes from hypoxic damage through
unknown signaling pathways. We tested the hypothesis that S1P-induced
cardioprotection requires activation by the 
-isoform of protein
kinase C (PKC) by subjecting hearts isolated from PKC knockout
mice and wild-type mice to 20 min of global ischemia and 30 min
of reperfusion. Pretreatment with a 2-min infusion of 10 nM S1P
improved recovery of left ventricular developed pressure (LVDP) in both
wild-type and PKC knockout hearts and reduced the rise in LV
end-diastolic pressure (LVEDP) and creatine kinase (CK) release.
Pretreatment for 2 min with 10 nM of the ganglioside GM-1 also improved
recovery of LVDP and suppressed CK release in wild-type hearts but not
in PKC knockout hearts. Importantly, GM-1 but not S1P, increased the
proportion of PKC localized to particulate fractions. Our results
suggest that GM-1, which enhances endogenous S1P production, reduces
cardiac injury through PKC-dependent intracellular pathways. In
contrast, extracellular S1P induces equivalent cardioprotection through PKC-independent signaling pathways.
ischemia-reperfusion injury; -isoform of protein kinase
C
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