BoneKEy Reports | BoneKEy Watch
Gap junctions mediate bone response to mechanical stress
DOI:10.1038/bonekey.2013.60
Using a modification of their ex vivo bone explant system, which has already demonstrated that osteocytes modulate calcium ion oscillations in intact bone through gap junctions, Ishihara et al. have now developed a fluid-flow platform to investigate the signaling pathways involved in the response to mechanical stress.
The system introduced fluid flow at the surface of the explanted bone and allowed calcium ion oscillations that occurred in response to mechanical stress to be assessed. When fluid flow was introduced, both osteoblasts and osteocytes showed a stress-induced calcium signaling response, and c-fos expression in the bone explants increased. When a specific and reversible gap-junction inhibitor was added to the system, the calcium signaling response to mechanical stress in osteoblasts was unaffected but the response to fluid flow was abolished in osteocytes. Blocking stretch-activated channels did not affect the response to mechanical stress observed in osteocytes and its effect on the response of osteoblasts was minimal.
Taken together, the results show that an autonomous calcium ion oscillatory response occurs to shear stress applied directly to bone via fluid flow. The response is mediated by communications that occur between cells at the gap junctions.
Editor’s comment: This ex vivo bone explant system demonstrated fluid-flow-induced activation of autonomous [Ca2+]i oscillation via gap-junction-mediated cell–cell communication and hemichannels. This imaging system may become a useful tool for examining the early signaling events that occur during mechanotransduction.
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