Mechanical injury increases eicosanoid production in cultured cardiomyocytes.
The release of three stable metabolites of the arachidonic acid cascade was determined in cultures of cardiac myocytes and of non-muscle cells. In both cell types, the main product was 6-keto-PGF1 alpha much less PGE2 was released, while TXB2 was only detected in muscle cells. Preincubation with arachidonic acid increased the release of all the PGs in both types of culture. Mechanical injury had a synergistic effect on the increased PG release in AA-preincubated cells. However, TXB2 was not detected in F-cells in any experimental conditions. These results suggest that PG production serves a functional role in heart preservation during injury.
Pinson
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A
Laboratory for Myocardial Research, Hebrew University-Hadassah Medical School, Jerusalem, Israel.
Halabi
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A
Shohami
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E
D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis; D000818:Animals; D001095:Arachidonic Acids / Q000378:metabolism; D002478:Cells, Cultured; D015232:Dinoprostone / Q000096:biosynthesis; D015777:Eicosanoids / Q000096:biosynthesis*; D006335:Heart Injuries / Q000378:metabolism; D009206:Myocardium / Q000166:cytology / Q000378:metabolism*; D051381:Rats; D013314:Stress, Mechanical; D013929:Thromboxane B2 / Q000096:biosynthesis
D001095:Arachidonic Acids; D015777:Eicosanoids; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; D015232:Dinoprostone