| 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
Yoshiko, Yuji
Kozai, Katsuyuki
Aubin, Jane E
Maeda, Norihiko
|
| 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 |
Bone_44_1177.pdf (2.3 MB)
