書誌事項
- タイトル別名
-
- Down-regulation of K<sub>Ca</sub>3.1 contribute to the antiproliferative effect of vitamin D receptor agonists in mouse preosteoblasts
抄録
<p>Vitamin D (VD) plays important roles in bone development indirectly via control calcium absorption in the intestine and reabsorption in the kidney. However, several in vitro studies showed that VD can directly suppress the cell proliferation of mouse osteoblasts. The intermediate-conductance Ca2+-activated K+ channel KCa3.1 regulates intracellular Ca2+ signaling pathways and is associated with cell proliferation in various types of cells. In the present study, treatment with VDR agonists for 48 h markedly decreased the expression levels of KCa3.1 transcripts and proteins in mouse preosteoblast MC3T3-E1 cells, resulting in the significant inhibition of Ca2+ rises induced by DCEBIO, a specific KCa3.1 activator. Treatments with VDR agonists also significantly decreased the expression of transcriptional regulators of KCa3.1 such as histone deacetylase 2 (HDAC2) and Fra-1 composed of activation protein 1. In addition, the siRNA-mediated blockade of VDR significantly rescued the decreased expression of KCa3.1, HDAC2, and Fra-1 protein in MC3T3-E1 cells treated with VDR agonists. Our results suggest that KCa3.1 is a new downstream target of VDR signaling and the down-regulation of KCa3.1 contributes, at least partly, to the antiproliferative effect of VDR agonists in mouse pre-osteoblasts.</p>
収録刊行物
-
- 日本薬理学会年会要旨集
-
日本薬理学会年会要旨集 93 (0), 2-P-242-, 2020
公益社団法人 日本薬理学会
- Tweet
詳細情報 詳細情報について
-
- CRID
- 1390565134836803072
-
- NII論文ID
- 130007811709
-
- ISSN
- 24354953
-
- 本文言語コード
- ja
-
- データソース種別
-
- JaLC
- Crossref
- CiNii Articles
-
- 抄録ライセンスフラグ
- 使用不可