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 Tools annual

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 monthly

Global: Zendy Plus monthly

Presents the access of premium content as premium feature

Premium Content

Global: Zendy Plus annual

Global: Zendy Free Plan

Aims  The local concentration of extracellular Ca 2+  ([Ca 2+ ] o ) in bone microenvironment is accumulated during bone remodeling. In the present study we investigated whether elevating [Ca 2+ ] o  induced store-operated calcium entry (SOCE) in primary rat calvarial osteoblasts and further examined the contribution of elevating [Ca 2+ ] o  to osteoblastic proliferation.    Methods  Cytosolic Ca 2+  concentration ([Ca 2+ ] c ) of primary cultured rat osteoblasts was detected by fluorescence imaging using calcium-sensitive probe fura-2/AM. Osteoblastic proliferation was estimated by cell counting, MTS assay and ATP assay. Agonists and antagonists of calcium-sensing receptors (CaSR) as well as inhibitors of phospholipase C (PLC), SOCE and voltage-gated calcium (Cav) channels were applied to study the mechanism in detail.    Results  Our data showed that elevating [Ca 2+ ] o  evoked a sustained increase of [Ca 2+ ] c  in a dose-dependent manner. This [Ca 2+ ] c  increase was blocked by TMB-8 (Ca 2+  release inhibitor), 2-APB and BTP-2 (both SOCE blockers), respectively, whereas not affected by Cav channels blockers nifedipine and verapamil. Furthermore, NPS2143 (a CaSR antagonist) or U73122 (a PLC inhibitor) strongly reduced the [Ca 2+ ] o -induced [Ca 2+ ] c  increase. The similar responses were observed when cells were stimulated with CaSR agonist spermine. These data indicated that elevating [Ca 2+ ] o  resulted in SOCE depending on the activation of CaSR and PLC in osteoblasts. In addition, high [Ca 2+ ] o  significantly promoted osteoblastic proliferation, which was notably reversed by BAPTA-AM (an intracellular calcium chelator), 2-APB, BTP-2, TMB-8, NPS2143 and U73122, respectively, but not affected by Cav channels antagonists.    Conclusions  Elevating [Ca 2+ ] o  induced SOCE by triggering the activation of CaSR and PLC. This process was involved in osteoblastic proliferation induced by high level of extracellular Ca 2+  concentration.

plos one

Elevation of Extracellular Ca2+ Induces Store-Operated Calcium Entry via Calcium-Sensing Receptors: A Pathway Contributes to the Proliferation of Osteoblasts