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Articles in PresS, published online ahead of print February 14, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.01029.2001
Submitted on November 27, 2001
Accepted on February 12, 2002
PKC knockout mouse hearts
1 Cardiology, VA Medical Center, San Francisco, CA, USA; Medicine, University of California, San Francisco, CA, USA
2 Cardiology, VA Medical Center, San Francisco, CA, USA
3 Molecular Pharmacology, Stanford University, Stanford, CA, USA
4 Research Center, Ernest Gallo, Emeryville, CA, USA; Medicine, University of California, San Francisco, CA, USA
5 Medicine, University of California, San Francisco, CA, USA
* To whom correspondence should be addressed. E-mail: joel.karliner{at}med.va.gov.
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 protein kinase C (PKC) activation by subjecting hearts isolated from PKC knockout mice and wild-type mice to 20 min global ischemia and 30 min 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 recocvery of LVDP and supressed 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 cadiac injury through PKC-dependent intracellular pathways. In contrast, extracellular S1P induces equivalent cardioprotection through PKC-indpendent signaling pathways.
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