Integrin β1 overexpression protects nucleus pulposus cells from apoptosis and attenuates intervertebral disc degeneration

Intervertebral disc (IVD) degeneration is a chronic pathologic process characterized by excessive apoptosis of intervertebral disc cells. The purpose of the current study was to detect the effect of integrin β1 on apoptosis of NP cells and IVD degeneration. Integrin β1 overexpressing lentivirus vector (LV-ITG β1) was constructed and transduced to NP cells, and its effect on cell apoptosis were studied in vitro. The underlying mechanism was subsequently studied. In addition, the in vivo effect of integrin β1 on IVD degeneration was studied by intradiscal injection of LV-ITG β1 in a rat IVD degeneration model. In vitro study showed that integrin β1 overexpression protected NP cells from levofloxacin-induced apoptosis, and LV-ITG β1 could significantly upregulate the expression of both FAK and p-FAK and downregulate the expression of P53 measured by western blot. Intradiscal injections of LV-ITG β1 suppressed NP cell apoptosis tested by TUNEL staining, and attenuated disc degeneration assessed by histological and MRI examination. Our findings suggested that integrin β1 could be used as an effective gene therapy target for IVD degeneration due to its significant effect on preventing NP cell apoptosis both in vitro and in vivo, and FAK-P53 signaling axial was involved in the protective effect of integrin β1 on NP cells.