There is great confusion in the literature on mechano-transduction in osteoblasts. This is partly due to the use of hyper and hypophysiological systems for applying forces to cells. We only find evidence for the role of ion channels at hyper-physiological levels of strain. The cells are far more sensitive to tension than compression indicating that structures within the cell are decisive in determining response and that there is no tensegrity within the cell. Single cell mechanical measurements using an adapted atomic force microscope built in our lab, also does not show any evidence for a tensegrity structure. Analysis of the dimension of stretch and the amount of force needed to activate cells indicates that stretch activated ion channels are not involved as the force required is extremely high in relation to the activation energy of an ion channel. The force required to activate at the mechanosensing system is more in line with the forces generated inside a cell by the actin-myosin structure of several hundred thousand piconewtons.

We find no evidence for any other pathway than a PLC-PKC-Calcium pathway involved in any of the signal transduction pathways, but other pathways are involved in hyperphysiological stretch. One of these induces ICAM-1 and thus can induce inflammatory pathways through cell-cell binding of macrophages and other cells.

Due to the very high energies involved in activating the mechano-transduction pathways we do not see any graviception mechanism of single cells. Indeed many microgravitx flights of 25 seconds duration and a flight of 6 minutes did not show any effect in intracellular calcium. The cellular response to microgravity, if it is not an artefact, is not related to mechanosensing.

This work was supported by the German Space Agency (DLR)