TAZ enhances the activity of the AKT signaling pathway to promote adipogenesis of gADSCs.

Adipose-derived mesenchymal stem cells (ADSCs) possess the capacity for multidirectional differentiation, including differentiation into adipocytes. However, the molecular mechanisms that control adipogenesis are not yet fully understood.Transcriptional co-activator with PDZ-binding motif (TAZ) can act as a molecular rheostat, finely regulating the balance between osteoblast and adipocyte differentiation. In this study, we investigated whether TAZ plays a role in the adipogenesis of goat ADSCs (gADCS). Our results indicated that the expression of TAZ increased during adipogenesis of gADSCs. We established gADSCs cell lines with stable TAZ overexpression and knockdown. We found that TAZ overexpression promoted the adipogenesis of gADSCs, whereas its knockdown inhibited this process. Furthermore, TAZ overexpression and knockdown altered the nuclear expression of Yes-associated protein(YAP) and TAZ. Subsequent analyses indicated that TAZ overexpression increased AKT phosphorylation levels. Moreover, treatment with a PI3K inhibitor (LY294002) abrogated the TAZ-induced increase in adipogenesis, suggesting that TAZ regulates the adipogenesis of gADSCs via the PI3K/AKT pathway. Collectively, our results indicate that TAZ promotes the adipogenesis of gADSCs by enhancing the activity of the PI3K/AKT signaling pathway.