Photoactivation of TAZ via Akt/GSK3β signaling pathway promotes osteogenic differentiation.

Osteogenesis disorder is involved in osteoporosis and other related bone diseases, in which osteogenic differentiation is essential. Osteogenic differentiation is a complicated process regulated by intricate signal transduction networks. It has been reported that low-power laser irradiation (LPLI) has an osteogenic potential by promoting osteoblast differentiation. However, the molecular mechanisms remain to be understood. In this study, we reveal a novel mechanism that Akt/GSK3β/TAZ (transcriptional co-activator with PDZ-binding motif) signaling pathway plays a crucial role in LPLI-enhanced osteoblast differentiation. Photomodulation by LPLI activated Akt/GSK3β pathway which inhibited TAZ phosphorylation, leading to the increase of TAZ protein level and nuclear aggregation. Meanwhile, knockdown of TAZ suppressed osteogenic differentiation promoted by LPLI. Further study showed that LPLI promoted the interaction between TAZ and core-binding factor 1 (Cbfa1), up-regulating the transcription of osteopontin (OPN) and osteocalcin (OCN) and the activity of alkaline phosphatase (ALP). However, inhibition of Akt/GSK3β pathway reversed the effects of TAZ on osteogenic differentiation induced by LPLI. Taken together, for the first time, we report that LPLI promotes osteoblast differentiation via TAZ activation dependent on Akt/GSK3β signaling pathway.