2022, Vol. 26 ›› Issue (17): 2726-2731
Bone morphogenetic protein 7 inhibits apoptosis of nucleus pulposus cells
Disc degeneration is one of the major causes of lower back pain, and current clinical surgical treatments can relieve painful symptoms but sacrifice disc function and cannot completely cure disc degeneration. Therefore, it is important to develop new biological treatments to curb the progression of early disc degeneration, or to regenerate degenerated disc tissue.
To investigate whether bone morphogenetic protein 7 can reduce the senescence of human nucleus pulposus cells during subculture and its possible mechanism.
Patients who underwent discectomy were enrolled in this study. During the operation, the intervertebral disc tissue was obtained and human nucleus pulposus cells were extracted and subcultured in vitro for six times. The cells were then cultured with bone morphogenetic protein 7 or LY294002, a specific inhibitor of phosphatidyl-inositol 3-kinase. Cell proliferation ability, telomerase activity, β-galactosidase activity, and the expression of apoptosis-related genes and phosphatidyl-inositol 3-kinase/protein kinase B signaling pathway molecules were detected.
Bone morphogenetic protein 7 could significantly increase the cell proliferation and telomerase activity of nucleus pulposus cells, decrease the activity of β-galactosidase, down-regulate the expression of p16 and p53, and activate phosphatidyl-inositol 3-kinase/protein kinase B signaling pathway. In addition, LY294002 could significantly reverse the anti-apoptotic effect of bone morphogenetic protein 7 on nucleus pulposus cells. Overall, bone morphogenetic protein 7 exerts the anti-apoptotic effect on nucleus pulposus cells by activating the phosphatidyl-inositol 3-kinase/protein kinase B signaling pathway. The results of this study can provide new knowledge for in vitro culture and tissue engineering of allogenic nucleus pulposus cells.
intervertebral disc regeneration, nucleus pulposus cells, bone morphogenetic protein 7, apoptosis