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 PLA 2 inhibitor, suppressed the thrombin-induced AA release. In addition, quinacrine also suppressed the thrombin-induced prostaglandin E 2 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 E 2 synthesis. These results strongly suggest that thrombin induces AA release not by phosphatidylcholine hydrolysis by PLD nor phosphoinositide hydrolysis by PLC but mainly by PLA 2 in osteoblast-like cells.
| Original language | English |
|---|---|
| Pages (from-to) | 467-472 |
| Number of pages | 6 |
| Journal | Prostaglandins Leukotrienes and Essential Fatty Acids |
| Volume | 56 |
| Issue number | 6 |
| DOIs | |
| Publication status | Published - 01-01-1997 |
| Externally published | Yes |
Fingerprint
All Science Journal Classification (ASJC) codes
- Clinical Biochemistry
- Cell Biology
Cite this
}
Mechanism of thrombin-induced arachidonic acid release in osteoblast-like cells. / Suzuki, Atsushi; Kozawa, O.; Shinoda, J.; Watanabe-Tomita, Y.; Saito, H.; Oiso, Y.
In: Prostaglandins Leukotrienes and Essential Fatty Acids, Vol. 56, No. 6, 01.01.1997, p. 467-472.Research output: Contribution to journal › Article
TY - JOUR
T1 - Mechanism of thrombin-induced arachidonic acid release in osteoblast-like cells
AU - Suzuki, Atsushi
AU - Kozawa, O.
AU - Shinoda, J.
AU - Watanabe-Tomita, Y.
AU - Saito, H.
AU - Oiso, Y.
PY - 1997/1/1
Y1 - 1997/1/1
N2 - 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 PLA 2 inhibitor, suppressed the thrombin-induced AA release. In addition, quinacrine also suppressed the thrombin-induced prostaglandin E 2 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 E 2 synthesis. These results strongly suggest that thrombin induces AA release not by phosphatidylcholine hydrolysis by PLD nor phosphoinositide hydrolysis by PLC but mainly by PLA 2 in osteoblast-like cells.
AB - 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 PLA 2 inhibitor, suppressed the thrombin-induced AA release. In addition, quinacrine also suppressed the thrombin-induced prostaglandin E 2 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 E 2 synthesis. These results strongly suggest that thrombin induces AA release not by phosphatidylcholine hydrolysis by PLD nor phosphoinositide hydrolysis by PLC but mainly by PLA 2 in osteoblast-like cells.
UR - http://www.scopus.com/inward/record.url?scp=0030922041&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0030922041&partnerID=8YFLogxK
U2 - 10.1016/S0952-3278(97)90601-3
DO - 10.1016/S0952-3278(97)90601-3
M3 - Article
VL - 56
SP - 467
EP - 472
JO - Prostaglandins Leukotrienes and Essential Fatty Acids
JF - Prostaglandins Leukotrienes and Essential Fatty Acids
SN - 0952-3278
IS - 6
ER -