Spaceflight and bed rest induce loss of bone
mass. A number of in vivo and in vitro studies have
been conducted to clarify the mechanisms, however,
the results have been conflicting. The purpose
of this study was to investigate the effects of
gravity unloading on proliferation, phenotypes,
and apoptosis of normal human osteoblastic cells
in the presence of 1α,25-dihydroxyvitamin D
3. We
used a vector-averaged gravity condition generated
by clinostat rotation to simulate gravity unloading.
Clinostat rotation did not affect the cell proliferation.
On the first day, the mRNA levels for osteocalcin,
ALP, CBFA1, VDR, RANKL, and OPG were
reduced by clinostat rotation to 21%, 65%, 62%,
52%, 43%, and 54% of control, respectively. ALP
activity was decreased to 75% of control. On the
second day, the mRNA levels for osteocalcin and
RANKL were reduced to 77% and 61% of control,
respectively. The decreased VDR mRNA level
might be responsible for the reduction for mRNA
levels for osteocalcin, RANKL, and OPG. Clinostat
rotation increased the pro-apoptotic index
(Bax/Bcl-2 ratio) but did not induce apoptosis due
to the simultaneous upregulation of the anti-apoptotic
XIAP. Reduction of osteoblast responsiveness
to 1α,25-dihydroxyvitamin D
3 might be involved in
osteopenia that is induced by gravity unloading.
抄録全体を表示