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2017 Fiscal Year Final Research Report

Role of Ca2+ signaling due to the activation of K+ channels in bone remodeling

Research Project

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Project/Area Number 16K21474
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Pharmacology in pharmacy
Biological pharmacy
Research InstitutionNagoya City University (2017)
Kyoto Pharmaceutical University (2016)

Principal Investigator

Kito Hiroaki  名古屋市立大学, 大学院医学研究科, 助教 (40749181)

Project Period (FY) 2016-04-01 – 2018-03-31
Keywords薬理学 / パッチクランプ法 / カルシウム活性化カリウムチャネル / VDR / 前骨芽細胞
Outline of Final Research Achievements

In present study, we showed that KCa3.1 were functionally expressed in mouse preosteoblast MC3T3-E1, and the activation of KCa3.1 promoted the cell growth of MC3T3-E1 cells. To clarify the physiological function of KCa3.1 in MC3T3-E1 cells, contribution of KCa3.1 to VDR agonists-induced suppression of cell proliferation were examined. Treatments with VDR agonists markedly decreased the expression levels of KCa3.1 transcripts and proteins in MC3T3-E1 cells. Treatments with VDR agonists also significantly decreased the expression of several transcriptional regulators of KCa3.1 such as histone deacetylase 2 (HDAC2) and Fra-1 composed of activation protein 1. Our results suggest that KCa3.1 is a new downstream target of VDR signaling and the down-regulation of KCa3.1 through the transcriptional repression of KCa3.1 contribute, at least partly, to the antiproliferative effects of VDR agonists in mouse pre-osteoblasts.

Free Research Field

薬理学

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Published: 2019-03-29  

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