In the current study, we examined the role of gap junctions in oscillatory
fluid flow-induced changes in intracellular Ca2+ concentration and prostagl
andin release in osteoblastic cells. This work was completed in MC3T3-E1 ce
lls with intact gap junctional communication as well as in MC3T3-E1 cells r
endered communication deficient through expression of a dominant-negative c
onnexin. Our results demonstrate that MC3T3-E1 cells with intact gap juncti
ons respond to oscillatory fluid flow with significant increases in prostag
landin E-2 (PGE(2)) release, whereas cells with diminished gap junctional c
ommunication do not. Furthermore, we found that cytosolic Ca2+ (Ca-i(2+)) r
esponse was unaltered by the disruption in gap junctional communication and
was not significantly different among the cell lines. Thus our results sug
gest that gap junctions contribute to the PGE(2) but not to the Ca-i(2+) re
sponse to oscillatory fluid flow. These findings implicate gap junctional i
ntercellular communication (GJIC) in bone cell ensemble responsiveness to o
scillatory fluid flow and suggest that gap junctions and GJIC play a pivota
l role in mechanotransduction mechanisms in bone.