Role of Ca2+ signaling due to the activation of K+ channels in bone remodeling
| Project/Area Number |
16K21474
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pharmacology in pharmacy
Biological pharmacy
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| Research Institution | Nagoya City University (2017)
Kyoto Pharmaceutical University (2016) |
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Principal Investigator |
Kito Hiroaki 名古屋市立大学, 大学院医学研究科, 助教 (40749181)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| 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 / イオンチャネル / VDR / 骨芽細胞 / 破骨細胞 / 細胞増殖 / カリウムチャネル |
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| 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.
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Report
(3 results)
Research Products
(16 results)
