Endothelin-1 Stimulates Secretion of Lipoprotein Lipase from Ehrlich Ascites Tumor Cells
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- Kerakawati Rie
- Department of Biochemistry, Faculty of Pharmacy and Pharmaceutical Sciences, Fukuyama University
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- Morita Tetsuo
- Department of Biochemistry, Faculty of Pharmacy and Pharmaceutical Sciences, Fukuyama University
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抄録
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.
収録刊行物
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- JOURNAL OF HEALTH SCIENCE
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JOURNAL OF HEALTH SCIENCE 56 (4), 467-471, 2010
公益社団法人 日本薬学会
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詳細情報 詳細情報について
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- CRID
- 1390282679473831808
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- NII論文ID
- 130000303547
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- NII書誌ID
- AA11316464
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- ISSN
- 13475207
- 13449702
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- NDL書誌ID
- 10764241
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
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