Browse

High Extracellular Calcium Increased Expression of Ank, PC-1 andOsteopontin in Mouse Calvarial Cells

Cited 0 time in Web of Science Cited 0 time in Scopus
Authors
Kim, Gwan-Shik; Song, Mina; Ryoo, Hyun-Mo; Woo, Kyung-Mi; Baek, Jeong-Hwa
Issue Date
2008-03
Publisher
Korean Academy of Oral Biology
Citation
International Journal of Oral Biology 33:33-43
Keywords
high extracellular calciumosteoblastmatrix calcificationAnkPC-1Osteopontin
Abstract
In the process of bone remodeling, mineral phase of bone
is dissolved by osteoclasts, resulting in elevation of calcium
concentration in micro-environment. This study was performed
to explore the effect of high extracellular calcium
(Ca
2+
e) on mineralized nodule formation and on the expression
of progressive ankylosis (Ank), plasma cell membrane
glycoprotein-1 (PC-1) and osteopontin by primary cultured
mouse calvarial cells. Osteoblastic differentiation and mineralized
nodule formation was induced by culture of mouse
calvarial cells in osteoblast differentiation medium containing
ascorbic acid and β-glycerophosphate. Although Ank, PC-1
and osteopontin are well known inhibitors of mineralization,
expression of these genes were induced at the later stage of
osteoblast differentiation during when expression of osteocalcin,
a late marker gene of osteoblast differentiation, was
induced and mineralization was actively progressing. High
Ca
2+
e (10 mM) treatment highly enhanced mRNA expression
of Ank, PC-1 and osteopontin in the late stage of osteoblast
differentiation but not in the early stage. Inhibition of p44/42
MAPK activation but not that of protein kinase C suppressed
high Ca
2+
e-induced expression of Ank, PC-1 and
osteopontin. When high Ca
2+
e (5 mM or 10 mM) was present
in culture medium during when mineral deposition was
actively progressing, matrix calcifiation was significantly
increased by high Ca
2+
e. This stimulatory effect was abolished
by pyrophosphate (5 mM) or levamisole (0.1-0.5 mM), an
alkaline phosphatase inhibitor. In addition, probenecid (2mM),
an inhibitor of Ank, suppressed matrix calcification in both
control and high Ca
2+
e-treated group, suggesting the possible
role of Ank in matrix calcification by osteoblasts. Taken
together, these results showed that high Ca
2+
e stimulates expression of Ank, PC-1 and osteopontin as well as matrix
calcification in late differentiation stage of osteoblasts and
that p44/42 MAPK activation is involved in high Ca
2+
e-
induced expression of Ank, PC-1 and osteopontin.
ISSN
1226-7155
Language
Korean
URI
https://hdl.handle.net/10371/68816
Files in This Item:
Appears in Collections:
College of Dentistry/School of Dentistry (치과대학/치의학대학원)Dept. of Dentistry (치의학과)Journal Papers (저널논문_치의학과)
  • mendeley

Items in S-Space are protected by copyright, with all rights reserved, unless otherwise indicated.

Browse