Arachidonic acid release induced by extracellular ATP in osteoblasts: Role of phospholipase D

Y. Watanabe-Tomita, Atsushi Suzuki, J. Shinoda, Y. Oiso, O. Kozawa

研究成果: Article

16 引用 (Scopus)

抄録

In a previous study, we have shown that extracellular ATP stimulates Ca2+ influx resulting in the release of arachidonic acid (AA) and prostaglandin E2 (PGE2) synthesis in osteoblast-like MC3T3-E1 cells. In addition, we have recently reported that extracellular ATP stimulates phosphatidylcholine hydrolysis by phospholipase D (PLD) independently from the activation of protein kinase C in these cells. It is well recognized that phosphatidylcholine is hydrolysed by PLD, generating phosphatidic acid, which can be further degraded by phosphatidic acid phosphohydrolase to diacylglycerol (DG). In the present study, we investigated the role of PLD activation in the extracellular ATP-induced AA release and PGE2 synthesis in osteoblast-like MC3T3-E1 cells. Extracellular ATP stimulated AA release dose-dependently in the range between 0.1 and 1 mM. Propranolol, which is known to inhibit phosphatidic acid phosphohydrolase, significantly inhibited the AA release induced by extracellular ATP in a dose-dependent manner in the range between 100 and 300 μM. 1,6-Bis-(cyclohexyloximinocarbonylamino)(RHC-80267), a selective inhibitor of DG lipase, significantly suppressed the AA release induced by extracellular ATP. Both the pretreatment of propranolol and RHC-80267 also inhibited the extracellular ATP-induced PGE2 synthesis. These results strongly suggest that the AA release induced by extracellular ATP is mediated at [east in part by phosphatidylcholine hydrolysis by PLD in osteoblast-like cells.

元の言語English
ページ(範囲)335-339
ページ数5
ジャーナルProstaglandins Leukotrienes and Essential Fatty Acids
57
発行部数3
DOI
出版物ステータスPublished - 01-01-1997
外部発表Yes

Fingerprint

Phospholipase D
Osteoblasts
Arachidonic Acid
Adenosine Triphosphate
Phosphatidylcholines
Phosphatidate Phosphatase
Dinoprostone
Propranolol
Hydrolysis
Chemical activation
Phosphatidic Acids
Lipoprotein Lipase
Diglycerides
Protein Kinase C

All Science Journal Classification (ASJC) codes

  • Clinical Biochemistry
  • Cell Biology

これを引用

@article{4c782615ed624165b5a8b66eb8dfbacd,
title = "Arachidonic acid release induced by extracellular ATP in osteoblasts: Role of phospholipase D",
abstract = "In a previous study, we have shown that extracellular ATP stimulates Ca2+ influx resulting in the release of arachidonic acid (AA) and prostaglandin E2 (PGE2) synthesis in osteoblast-like MC3T3-E1 cells. In addition, we have recently reported that extracellular ATP stimulates phosphatidylcholine hydrolysis by phospholipase D (PLD) independently from the activation of protein kinase C in these cells. It is well recognized that phosphatidylcholine is hydrolysed by PLD, generating phosphatidic acid, which can be further degraded by phosphatidic acid phosphohydrolase to diacylglycerol (DG). In the present study, we investigated the role of PLD activation in the extracellular ATP-induced AA release and PGE2 synthesis in osteoblast-like MC3T3-E1 cells. Extracellular ATP stimulated AA release dose-dependently in the range between 0.1 and 1 mM. Propranolol, which is known to inhibit phosphatidic acid phosphohydrolase, significantly inhibited the AA release induced by extracellular ATP in a dose-dependent manner in the range between 100 and 300 μM. 1,6-Bis-(cyclohexyloximinocarbonylamino)(RHC-80267), a selective inhibitor of DG lipase, significantly suppressed the AA release induced by extracellular ATP. Both the pretreatment of propranolol and RHC-80267 also inhibited the extracellular ATP-induced PGE2 synthesis. These results strongly suggest that the AA release induced by extracellular ATP is mediated at [east in part by phosphatidylcholine hydrolysis by PLD in osteoblast-like cells.",
author = "Y. Watanabe-Tomita and Atsushi Suzuki and J. Shinoda and Y. Oiso and O. Kozawa",
year = "1997",
month = "1",
day = "1",
doi = "10.1016/S0952-3278(97)90553-6",
language = "English",
volume = "57",
pages = "335--339",
journal = "Prostaglandins Leukotrienes and Essential Fatty Acids",
issn = "0952-3278",
publisher = "Churchill Livingstone",
number = "3",

}

Arachidonic acid release induced by extracellular ATP in osteoblasts : Role of phospholipase D. / Watanabe-Tomita, Y.; Suzuki, Atsushi; Shinoda, J.; Oiso, Y.; Kozawa, O.

:: Prostaglandins Leukotrienes and Essential Fatty Acids, 巻 57, 番号 3, 01.01.1997, p. 335-339.

研究成果: Article

TY - JOUR

T1 - Arachidonic acid release induced by extracellular ATP in osteoblasts

T2 - Role of phospholipase D

AU - Watanabe-Tomita, Y.

AU - Suzuki, Atsushi

AU - Shinoda, J.

AU - Oiso, Y.

AU - Kozawa, O.

PY - 1997/1/1

Y1 - 1997/1/1

N2 - In a previous study, we have shown that extracellular ATP stimulates Ca2+ influx resulting in the release of arachidonic acid (AA) and prostaglandin E2 (PGE2) synthesis in osteoblast-like MC3T3-E1 cells. In addition, we have recently reported that extracellular ATP stimulates phosphatidylcholine hydrolysis by phospholipase D (PLD) independently from the activation of protein kinase C in these cells. It is well recognized that phosphatidylcholine is hydrolysed by PLD, generating phosphatidic acid, which can be further degraded by phosphatidic acid phosphohydrolase to diacylglycerol (DG). In the present study, we investigated the role of PLD activation in the extracellular ATP-induced AA release and PGE2 synthesis in osteoblast-like MC3T3-E1 cells. Extracellular ATP stimulated AA release dose-dependently in the range between 0.1 and 1 mM. Propranolol, which is known to inhibit phosphatidic acid phosphohydrolase, significantly inhibited the AA release induced by extracellular ATP in a dose-dependent manner in the range between 100 and 300 μM. 1,6-Bis-(cyclohexyloximinocarbonylamino)(RHC-80267), a selective inhibitor of DG lipase, significantly suppressed the AA release induced by extracellular ATP. Both the pretreatment of propranolol and RHC-80267 also inhibited the extracellular ATP-induced PGE2 synthesis. These results strongly suggest that the AA release induced by extracellular ATP is mediated at [east in part by phosphatidylcholine hydrolysis by PLD in osteoblast-like cells.

AB - In a previous study, we have shown that extracellular ATP stimulates Ca2+ influx resulting in the release of arachidonic acid (AA) and prostaglandin E2 (PGE2) synthesis in osteoblast-like MC3T3-E1 cells. In addition, we have recently reported that extracellular ATP stimulates phosphatidylcholine hydrolysis by phospholipase D (PLD) independently from the activation of protein kinase C in these cells. It is well recognized that phosphatidylcholine is hydrolysed by PLD, generating phosphatidic acid, which can be further degraded by phosphatidic acid phosphohydrolase to diacylglycerol (DG). In the present study, we investigated the role of PLD activation in the extracellular ATP-induced AA release and PGE2 synthesis in osteoblast-like MC3T3-E1 cells. Extracellular ATP stimulated AA release dose-dependently in the range between 0.1 and 1 mM. Propranolol, which is known to inhibit phosphatidic acid phosphohydrolase, significantly inhibited the AA release induced by extracellular ATP in a dose-dependent manner in the range between 100 and 300 μM. 1,6-Bis-(cyclohexyloximinocarbonylamino)(RHC-80267), a selective inhibitor of DG lipase, significantly suppressed the AA release induced by extracellular ATP. Both the pretreatment of propranolol and RHC-80267 also inhibited the extracellular ATP-induced PGE2 synthesis. These results strongly suggest that the AA release induced by extracellular ATP is mediated at [east in part by phosphatidylcholine hydrolysis by PLD in osteoblast-like cells.

UR - http://www.scopus.com/inward/record.url?scp=0030657859&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030657859&partnerID=8YFLogxK

U2 - 10.1016/S0952-3278(97)90553-6

DO - 10.1016/S0952-3278(97)90553-6

M3 - Article

C2 - 9384525

AN - SCOPUS:0030657859

VL - 57

SP - 335

EP - 339

JO - Prostaglandins Leukotrienes and Essential Fatty Acids

JF - Prostaglandins Leukotrienes and Essential Fatty Acids

SN - 0952-3278

IS - 3

ER -