Fluoride
Affects Calcium Homeostasis and Osteogenic Transcription Factor Expressions
Through L-type Calcium Channels in Osteoblast Cell Line.
Author
information
Abstract
Osteoblast
L-type voltage-dependent calcium channels (VDCC) play important roles in
maintaining intracellular homeostasis and influencing multiple cellular
processes. In particular, they contribute to the activities and functions of
osteoblasts (OBs). In order to study how L-type VDCC modulate calcium ion
(Ca2+)
homeostasis and the expression of osteogenic transcription factors in OBs
exposed to fluoride, MC3T3-E1 cells were exposed to a gradient of concentrations
of fluoride (0, 2.0, 5.0, 10.0 mg/L) in combination with 10 μM nifedipine, a
specific inhibitor of VDCC, for 48 h. We examined messenger RNA (mRNA) and
protein levels of Cav1.2, the main subunit of VDCC, and c-fos, c-jun,
runt-related transcription factor 2 (Runx2), osterix (OSX), and intracellular
free Ca2+ ([Ca2+]i)
concentrations in MC3T3-E1 cells. Our results showed that [Ca2+]i
levels increased in a dose-dependent manner with increase in concentration of
fluoride. Meantime, results indicated that lower concentrations of fluoride
(less than 5 mg/L, especially 2 mg/L) can lead to high expression of Cav1.2 and
enhance osteogenic function, while high concentration of fluoride (10 mg/L) can
induce decreased Cav1.2 and osteogenic transcriptional factors in MC3T3E1 cells
exposed to fluoride. However, the levels of [Ca2+]i,
Cav1.2, c-fos, c-jun, Runx2, and OSX induced by fluoride were significantly
altered and even reversed in the presence of nifedipine. These results
demonstrate that L-type calcium channels play a crucial role in
Ca2+ homeostasis
and they affect the expression of osteogenic transcription factors in
fluoride-treated osteoblasts.
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