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EP2 and EP4 receptors differentially mediate MAPK pathways underlying anabolic actions of prostaglandin E-2 on bone formation in rat calvaria cell cultures

https://hiroshima.repo.nii.ac.jp/records/2006525
https://hiroshima.repo.nii.ac.jp/records/2006525
80295d69-c313-43b2-9091-6a8edad89d32
名前 / ファイル ライセンス アクション
Bone_44_1177.pdf Bone_44_1177.pdf (2.3 MB)
Item type デフォルトアイテムタイプ_(フル)(1)
公開日 2023-03-18
タイトル
タイトル EP2 and EP4 receptors differentially mediate MAPK pathways underlying anabolic actions of prostaglandin E-2 on bone formation in rat calvaria cell cultures
言語 en
作成者 Minamizaki, Tomoko

× Minamizaki, Tomoko

en Minamizaki, Tomoko

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Yoshiko, Yuji

× Yoshiko, Yuji

en Yoshiko, Yuji

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Kozai, Katsuyuki

× Kozai, Katsuyuki

en Kozai, Katsuyuki

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Aubin, Jane E

× Aubin, Jane E

en Aubin, Jane E

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Maeda, Norihiko

× Maeda, Norihiko

en Maeda, Norihiko

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アクセス権
アクセス権 open access
アクセス権URI http://purl.org/coar/access_right/c_abf2
権利情報
権利情報 Copyright (c) 2009 Elsevier Inc. All rights reserved.
主題
主題Scheme Other
主題 Selective EP agonists
主題
主題Scheme Other
主題 Rat calvaria cells
主題
主題Scheme Other
主題 Osteoblastogenesis
主題
主題Scheme Other
主題 MAPKs
主題
主題Scheme Other
主題 Prostaglandin E
主題
主題Scheme NDC
主題 490
内容記述
内容記述 Of the four prostaglandin (PG) E receptor subtypes (EP1-EP4), EP2 and EP4 have been proposed to mediate the anabolic action of PGE(2) on bone formation but comparative evaluation Studies of EPs on bone formation do not necessarily share a common mechanism, implying that their additional features including downstream MAPK pathways may be beneficial to resolve this issue. We systematically assessed the roles of EPs in the rat calvaria (RC) cell Culture model by using four selective EP agonists (EPAs). Consistent with relative expression levels of the respective receptors, multiple phenotypic traits of bone formation in vitro, including proliferation of nodule-associated cells, osteoblast market expression and mineralized nodule formation were upregulated not only by PGE(2) but equally by EP2A and EP4A, but not by EP1A and EP3A. EP2A and EP4A were effective when cells were treated chronically or pulse-treated during nascent nodule formation. EP2A and EP4A equally stimulated the endogenous PGE(2) production, while EP2A caused a greater increase in cAMP production and c-Fos gene expression compared to EP4A. EP2A and EP4A activated predominantly p38 MAPK and ERK respectively, while c-Jun N-terminal kinase (JNK) was equally activated by both agonists. SB203580 (p38 MAPK inhibitor) blocked the PGE(2) effect on mineralized nodule formation, while U0126 (ERK inhibitor) and dicumarol (JNK inhibitor) were less effective. PGE(2)-dependent phosphorylation of the MAPKs was affected not only by protein kinase (PK)A and PKC inhibitors but also by adenylate cyclase and PKC activators. Co-treatment of RC cells with EP2A or EP4A and bone morphogenetic protein (BMP)2, whose effects on bone nodule formation is known to be, in part, mediated through the PKA and p38 MAPK pathways, resulted in an additive effect on mineralized nodule formation. Further, PGE2, EP2A and EP4A did not increase BMP2/4 mRNA levels in RC cells, and EP2-induced phosphorylation of p38 MAPK was not eliminated by Noggin. These results Suggest that, in the RC cell m
言語 en
出版者
出版者 Elsevier Science Inc
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
資源タイプ journal article
出版タイプ
出版タイプ AO
出版タイプResource http://purl.org/coar/version/c_b1a7d7d4d402bcce
関連情報
識別子タイプ DOI
関連識別子 10.1016/j.bone.2009.02.010
関連情報
識別子タイプ DOI
関連識別子 http://dx.doi.org/10.1016/j.bone.2009.02.010
収録物識別子
収録物識別子タイプ ISSN
収録物識別子 8756-3282
収録物識別子
収録物識別子タイプ NCID
収録物識別子 AA10506985
開始ページ
開始ページ 1177
書誌情報 Bone
Bone

巻 44, 号 6, p. 1177-1185, 発行日 2009-06
旧ID 28887
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