TAZ accelerates osteogenesis differentiation of mesenchymal stem cells via targeting PI3K/Akt.

Abstract

To investigate the promoting effects of TAZ on the osteogenic differentiation of mesenchymal stem cells in a rat model of osteoporosis through the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signal. A total of 12 Sprague-Dawley (SD) rats were randomly divided into normal group (n=6) and model group (n=6). The rats in normal group were not given any treatment, while those in model group were used to establish a model of osteoporosis, and the bone mineral density (BMD) of the femur and lumbar in each group was detected. Then, the bone marrow mesenchymal stem cells were observed, of which those in normal group were divided into normal group and inhibitor group. The bone marrow mesenchymal stem cells in model group were enrolled as model group. Alkaline phosphatase (ALP) staining was adopted to observe the osteogenesis, cell counting kit-8 (CCK-8) was applied to determine the cell proliferation, and immunohistochemistry was performed to measure the expression of TAZ. Western blotting was utilized to detect the relative expressions of phosphorylated Akt (p-Akt) and bone morphogenetic protein 2 (BMP-2) proteins, and quantitative Polymerase Chain Reaction (qPCR) was used to measure the messenger ribonucleic acid (mRNA) expression of TAZ. The average optical density of ALP-positive cells was decreased remarkably in model group and inhibitor group compared with that in normal group (p<0.05), while the cell proliferation rate was increased notably in model group and inhibitor group. In comparison with normal group, model group and inhibitor group had evidently declined positive expression and mRNA expression of TAZ (p<0.05). The relative expressions of p-Akt and BMP-2 proteins in model group and inhibitor group were significantly lower than those in normal group (p<0.05). TAZ promotes the osteogenic differentiation of mesenchymal stem cells in the rat model of osteoporosis by repressing the PI3K/Akt signal.