Retracted: Effects of IGFBP3 gene silencing mediated inhibition of ERK/MAPK signaling pathway on proliferation, apoptosis, autophagy, and cell senescence in rats nucleus pulposus cells

Abstract

Objective Disc degeneration is the common life‐threatening disease characterized by flank pain. The gene expression of insulin‐like growth factor binding protein 3 (IGFBP3) is increased in patients with disc degeneration, however, its mechanism is still unknown. This study aimed to investigate the influence of IGFBP3 gene silencing mediated inhibition of extracellular signal‐related kinase (ERK)/mitogen‐activated protein kinase (MAPK) signaling on proliferation, apoptosis, autophagy, and cell senescence in rats nucleus pulposus (NP) cells. Methods The expression of IGFBP3 in disc NP of patients was assessed by real‐time PCR (RT‐PCR) and western blot. RT‐PCR, transwell assay, immunohistochemical staining, SA‐β‐Gal staining, and western blot were performed to explore the molecular mechanism of IGFBP3 in NP cell migration and invasion. Results In this study, IGFBP3 was highly expressed in disc NP of patients. With RT‐PCR, transwell assay, immunohistochemical staining, SA‐β‐Gal staining, and western blot, downregulated IGFBP3 could inhibit NP cells' migration and invasion by targeting the ERK/MAPK signaling pathway. Conclusion Our findings revealed that the inhibition of the ERK/MAPK pathway was mediated by IGFBP3 silencing that had effects on proliferation, apoptosis, autophagy, and cell senescence. Furthermore, our findings suggested the underlying mechanism of disc degeneration.

Overexpressed IGFBP5 promotes cell proliferation and inhibits apoptosis of nucleus pulposus derived from rats with disc degeneration through inactivating the ERK/MAPK axis

“…The extracellular signal‐regulated kinases/mitogen‐activated protein kinase (ERK/MAPK) is crucial for the cell growth and survival, which is a highly conserved pathway known commonly to modulate the diverse cellular procedures involving proliferation, differentiation, and survival . Also, it has been previously revealed that silenced IGFBP‐3 may regulate the ERK/MAPK axis to suppress the migration and invasion of NP cells . Besides, NP cells of the IVD live in an environment that has a limited vascular provision and generate energy via anaerobic glycolysis .…”

“…16,17 Also, it has been previously revealed that silenced IGFBP-3 may regulate the ERK/MAPK axis to suppress the migration and invasion of NP cells. 18 Besides, NP cells of the IVD live in an environment that has a limited vascular provision and generate energy via anaerobic glycolysis. 19 Previously, osmolarity affecting the matrix synthesis in NP was correlated with the MAPK axes.…”

Retracted: Erratum

“…In Chen, Zhou, and Xu (), the following error was published on page 9308.…”

Single-cell RNA-seq analysis reveals the Wnt/Ca2+ signaling pathway with inflammation, apoptosis in nucleus pulposus degeneration

“…Prostaglandin E synthase (PTGES) plays a critical role (by similarity) in inflammation, fever and pain [ 31 ]. The gene expression of insulin-like growth factor binding protein 3 (IGFBP3) is closely related to apoptosis, autophagy and cellular senescence in nucleus pulposus cells [ 32 ]. Similarly, in chondrocytes 5, we also found a number of related genes that were mainly highly expressed in NP-degenerative cells, which were GDF15, TRIB3 and TNFRSF10B.…”