Endothelin-1 Stimulates Secretion of Lipoprotein Lipase from Ehrlich Ascites Tumor Cells

Since the role of endothelin (ET)-1 in lipoprotein metabolism in tumor cells is unclear, we investigated the effect of ET-1 on the secretion of lipoprotein lipase (LPL) from mouse Ehrlich ascites tumor cells. ET-1 increased the secretion of LPL from these cells in a time-dependent manner. Two antagonists of ET-receptor type A (ET-A), namely, BQ123 and FR139317, inhibited the stimulatory effect of ET-1 on the secretion of LPL. However, an antagonist of ET-receptor type B (ET-B), BQ788, did not have any effect. Neomycin, a phospholipase C (PLC) inhibitor, and H-7, a protein kinase C (PKC) inhibitor, also suppressed the ET-1-stimulated secretion of LPL. ET-1 also increased PKC activity in tumor cells in a dose-dependent manner. These results imply that ET-1 stimulates secretion of LPL from tumor cells by stimulating the PLC-PKC signaling pathway through the ET-A receptor rather than the ET-B receptor.