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Hokkaido University Collection of Scholarly and Academic Papers >
Societies >
北海道歯学雑誌 >
第44巻 >
エストロゲンによる異なった受容体を介するマクロファージ様細胞のNa, K-ATPase活性促進作用
| Title: | エストロゲンによる異なった受容体を介するマクロファージ様細胞のNa, K-ATPase活性促進作用 |
| Other Titles: | The activation effects of estrogen on Na, K-ATPase activity
in a macrophage-like cell through different receptors |
| Authors: | 平沢, 宏太1 Browse this author | | 出山, 義昭2 Browse this author →KAKEN DB | | 吉村, 善隆3 Browse this author →KAKEN DB | | 野谷, 健二4 Browse this author | | 鈴木, 邦明5 Browse this author →KAKEN DB |
| Authors(alt): | Hirasawa, Kota1 | | Deyama, Yoshiaki2 | | Yoshimura, Yoshitaka3 | | Notani, Kenji4 | | Suzuki, Kuniaki5 |
| Issue Date: | 15-Sep-2023 |
| Publisher: | 北海道歯学会 |
| Journal Title: | 北海道歯学雑誌 |
| Volume: | 44 |
| Start Page: | 16 |
| End Page: | 25 |
| Abstract: | Many types of cells in the monocyte‒macrophage linage have been shown to be regulated by estrogen. In addition, a body of information suggests that the Na, K-ATPase pump could be a target of 17β-estradiol (E2) in various types of cells. In this study, we explored the effects of E2 on the Na, K-ATPase in macrophage-like RAW 264.7 cells. E2 treatment of RAW 264.7 cells led to biphasic stimulation of Na, K-ATPase activity: an early activation via the cell surface receptor GPR30 and a late upregulation by nuclear estrogen receptor (ER)-activated signals. Antagonization of GPR30 by G15 abolished E2-induced early activation of Na, K-ATPase, while inhibition of ER signals nullified its late upregulation of Na, K-ATPase activity in a dose-dependent manner. Furthermore, short-term treatment with E2 induced phosphorylation of the Na, K-ATPase α1- subunit at Tyr-10, which relied on was related to an increase i n the N a＋ affinity of Na, K-ATPase. These results illustrate the involvement of two diffe rent signaling pathways in the regulation of Na, K-ATPase by E2. |
| Type: | article |
| URI: | http://hdl.handle.net/2115/90488 |
| Appears in Collections: | 北海道歯学雑誌 > 第44巻
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