RETRACTED: TRAF2 gene silencing induces proliferation and represses apoptosis of nucleus pulposus cells in rats with intervertebral disc degeneration

Abstract

We aim to research the role of TRAF2 silencing in regulating proliferation and apoptosis of nucleus pulposus cells (NIPCs) in rats with intervertebral disc degeneration (IDD) through mediating NF-κB signaling pathway. Degenerative disc nucleus pulposus tissues and normal nucleus pulposus tissues were collected to compare the positive expression of TRAF2 protein by immunohistochemistry, and to compare TRAF2, NF-κB (P65) and NF-κB (P50) expression by RT-qPCR and Western blot. A rat model with IDD was replicated using fibrous ring needle method and then treated with TRAF2-siRNA to silence TRAF2. Then, pathological changes and apoptosis in nucleus pulposus tissues were observed. In vitro NIPCs were transfected with TRAF2-siRNA or NF-κB pathway activator (recombinant TNF-α), and then colony formation, proliferation, senescence and apoptosis of NIPCs were determined. Increased TRAF2 and NF-κB were found in nucleus pulposus tissues from IDD patients and rats. Silencing TRAF2 inactivated NF-κB signaling pathway and attenuated pathological damage and apoptosis in nucleus pulposus tissues of rats with IDD. In in-vitro NIPCs, knockdown of TRAF2 resulted in promoted proliferation and colony formation ability while suppressed senescence and apoptosi. The NF-κB pathway activator (recombinant TNF-α) reversed the phenotypic changes of NIPCs resulted from TRAF2 silence. Our study demonstrates that TRAF2 is highly expressed in IDD, and silencing of TRAF2 promotes NIPC proliferation and restrains the apoptosis in IDD.