English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

The maturity of osteoblasts by proliferation and differentiation in preosteoblasts is essential for maintaining bone homeostasis. The beneficial effects of vitamin D on bone homeostasis in mammals have been demonstrated experimentally and clinically. However, the direct actions of vitamin D on preosteoblasts remain to be fully elucidated. In this study, we found that the functional activity of intermediate-conductance Ca 2+ -activated K +  channels (K Ca 3.1) positively regulated cell proliferation in MC3T3-E1 cells derived from mouse preosteoblasts by enhancing intracellular Ca 2+  signaling. We examined the effects of treatment with vitamin D receptor (VDR) agonist on the expression and activity of K Ca 3.1 by real-time PCR examination, Western blotting, Ca 2+  imaging, and patch clamp analyses in mouse MC3T3-E1 cells. Following the downregulation of K Ca 3.1 transcriptional modulators such as Fra-1 and HDAC2, K Ca 3.1 activity was suppressed in MC3T3-E1 cells treated with VDR agonists. Furthermore, application of the K Ca 3.1 activator DCEBIO attenuated the VDR agonist-evoked suppression of cell proliferation rate. These findings suggest that a decrease in K Ca 3.1 activity is involved in the suppression of cell proliferation rate in VDR agonist-treated preosteoblasts. Therefore, K Ca 3.1 plays an important role in bone formation by promoting osteoblastic proliferation under physiological conditions.

american journal of physiology. cell physiology

Downregulation of the Ca2+-activated K+ channel KCa3.1 in mouse preosteoblast cells treated with vitamin D receptor agonist