Mechanism of thrombin-induced arachidonic acid release in osteoblast-like cells

A. Suzuki, O. Kozawa, J. Shinoda, Y. Watanabe-Tomita, H. Saito, Y. Oiso

Research output: Contribution to journalArticlepeer-review

4 Citations (Scopus)

Abstract

In a previous study, we have reported that thrombin stimulates phosphatidylcholine hydrolysis by phospholipase (PL) D, but has little effect on phosphoinositide hydrolysis by PLC in osteoblast-like MC3T3-E1 cells. In the present study, we investigated the mechanism of the thrombin-induced arachidonic acid (AA) release in MC3T3-E1 cells. Thrombin stimulated AA release dose dependently in the range between 0.1 and 1 U/ml. Quinacrine, a PLA2 inhibitor, suppressed the thrombin-induced AA release. In addition, quinacrine also suppressed the thrombin-induced prostaglandin E2 synthesis in these cells. On the other hand, propranolol, which is known to inhibit phosphatidic acid phosphohydrolase, did not affect the thrombin-induced AA release. 1(6-((17β-3-Methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1 H-pyrrole-1H-pyrrole-2,5-dione (U-73122), a PLC inhibitor, had no effect on the AA release by thrombin. In addition, 1,6-bis-(cyclohexyloximinocarbonylamino)-hexane (RHC-80267), a selective inhibitor of diacylglycerol lipase, had little effect on the thrombin-induced AA release. Neither propranolol, U-73122 nor RHC-80267 affect the thrombin-induced prostaglandin E2 synthesis. These results strongly suggest that thrombin induces AA release not by phosphatidylcholine hydrolysis by PLD nor phosphoinositide hydrolysis by PLC but mainly by PLA2 in osteoblast-like cells.

Original languageEnglish
Pages (from-to)467-472
Number of pages6
JournalProstaglandins Leukotrienes and Essential Fatty Acids
Volume56
Issue number6
DOIs
Publication statusPublished - 06-1997

All Science Journal Classification (ASJC) codes

  • Clinical Biochemistry
  • Cell Biology

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