Chromobox homolog 4 overexpression inhibits TNF-α-induced matrix catabolism and senescence by suppressing activation of the NF-κB signaling pathway in nucleus pulposus cells.

Intervertebral disc degeneration (IDD) is featured as enhanced catabolism of extracellular matrix (ECM) in the nucleus pulposus (NP), in which tumor necrosis factor-alpha (TNF-α)-related cell senescence is involved. Chromobox homolog protein 4 (CBX4) exhibits anti-inflammatory effects and shows promising therapeutic potential. Thus, in the present study, we explore the role of CBX4 in IDD.

Identification of key potential targets for TNF-α/TNFR1-related intervertebral disc degeneration by bioinformatics analysis.

Background: Bioinformatics analysis was performed on gene expression profile microarray data to identify the key genes activated through the TNF-α/TNFR1 signaling pathway in intervertebral disc degeneration (IDD). The common differentially expressed genes (co-DEGs) were calculated in nucleus pulposus (NP) cells and annulus fibrosus (AF) cells under TNF-α treatment or TNFR1 knockdown, which reveals the potential mechanism of TNF-α involvement in IDD and may provide new therapeutic targets for IDD.

Methods: Differentially expressed genes (DEGs) in TNF-α-treated or TNFR1-knockdown NP cells and AF cells were identified.

Nicotinamide Phosphoribosyl Transferase Controls NLRP3 Inflammasome Activity Through MAPK and NF-κB Signaling in Nucleus Pulposus Cells, as Suppressed by Melatonin.

Intervertebral disc degeneration (IDD) is characterized by an imbalance between matrix synthesis and degradation in intervertebral discs. However, the causes of this imbalance remain elusive. Previous studies revealed that NLRP3 inflammasome plays a vital role in IDD and nicotinamide phosphoribosyl transferase (NAMPT) is involved in matrix degradation induced by IL-1β.

Erdheim-Chester disease mimicking lumbar nerve schwannoma: case report and literature review.

Introduction: Erdheim-Chester disease (ECD) is a rare, non-Langerhans cell histiocytosis. The clinical spectrum of ECD is diverse, varying from asymptomatic focal lesion to life-threatening multisystem infiltration. Neurological manifestations of ECD are common, mostly due to the involvement of the central nerve system.

MicroRNA-145 overexpression attenuates apoptosis and increases matrix synthesis in nucleus pulposus cells.

Aims: Lower back pain is often associated with intervertebral disc degeneration (IDD), which results from a decrease in nucleus pulposus (NP) cells and an imbalance between the degradation and synthesis of extracellular matrix (ECM) components. Multiple microRNAs play crucial roles in the modulation of NP cell apoptosis and matrix degradation. miR-145 is an important microRNA related to degenerative diseases such as osteoarthritis.

Transcription factor 7-like 2 controls matrix degradation through nuclear factor κB signaling and is repressed by microRNA-155 in nucleus pulposus cells.

Aim: TCF7L2, a key transcription factor in the canonical Wnt pathway, plays a vital role in the matrix degradation of chondrocytes. However, it is unknown whether TCF7L2 is important in the matrix metabolism of inner gel-like nucleus pulposus (NP) cells; thus, the aim of this study was to explore the effect and mechanism of TCF7L2 in this process.

Methods: Western blotting and immunofluorescence analyses were used to observe TCF7L2 expression in rat and human NP tissues.

Development of a Virtual Reality Preoperative Planning System for Postlateral Endoscopic Lumbar Discectomy Surgery and Its Clinical Application.

Objective: Percutaneous endoscopic lumbar discectomy is an effective way to treat lumbar disc herniation. Traditional preoperative planning based on a 2-dimensional method by magnetic resonance/computed tomography may cause inaccuracy of puncture during surgery. We used virtual reality to stimulate a surgery environment and measured relevant 3-dimensional data.

MicroRNA-155 suppresses the catabolic effect induced by TNF-α and IL-1β by targeting C/EBPβ in rat nucleus pulposus cells.

Aim: miR-155 is a pro-inflammatory or anti-inflammatory factor depending on the cell type in which it is expressed. miR-155 controls apoptosis and matrix degradation in nucleus pulposus (NP) cells in vitro. The aim of this study is to explore the effect of miR-155 in vivo and further investigate the mechanism of miR-155 in vitro.