Background/Aims: Osteoarthritis (OA) is the most frequently occurring joint disease and characterized by degeneration of cartilage. As the unique cell type in cartilage, chondrocytes play a crucial role during OA. Our study explored the influence of long non-coding RNA (lncRNA) growth arrest-specific transcript 5 (GAS5) on lipopolysaccharides (LPS)-induced injury in ATDC5 cells. Methods: Cell viability, apoptosis and expression of inflammatory cytokines were all assessed to evaluate LPS-induce inflammatory injury. Expression of GAS5 in LPS-induced cells was evaluated by qRT-PCR. After cell transfection, effect of abnormally expressed GAS5 on LPS-induced inflammatory injury was determined. Then, the possible target of GAS5 was screened by bioinformatics and verified by qRT-PCR and luciferase activity assay. Together, whether aberrant expression of target gene affected the modulation of GAS5 in LPS-induced inflammatory injury was also assessed. Finally, the influences of aberrant expressed Kruppel-like factor 2 (KLF2) on nuclear factor κB (NF-κB) and Notch pathways were detected by Western blot analysis. Results: LPS reduced cell viability and promoted cell apoptosis and secretion of inflammatory cytokines, along with down-regulation of GAS5. LPS-induced injury was alleviated by GAS5 overexpression while was exacerbated by GAS5 silence. KLF2 was predicted and verified as a target of GAS5, and GAS5 functioned through regulating expression of KLF2. Besides, aberrant expression of KLF2 regulated expressions of key kinases involved in the NF-κB and Notch pathways. Conclusion: GAS5 might ameliorate LPS-induced inflammatory injury in ATDC5 chondrocytes by inhibiting the NF-κB and Notch signaling pathways.

Posterior lumbar spinal fusion has been widely used in degenerative lumbar stenosis, but adjacent segment degeneration (ASD) was common. Researchers have found many risk factors for ASD after one or two levels of surgery, but few clinical studies focused on multi-level surgery. The purpose of this study was to clarify risk factors for upper ASD after multi-level posterior lumbar spinal fusion. A retrospective study was performed on the clinical data of 71 patients with degenerative lumbar stenosis who underwent multi-level (at least 3 levels) posterior lumbar spinal fusion from January 2013 to December 2016. Two groups were divided according to lamina and posterior ligamentous complex (PLC) maintenance of proximal fixed vertebrae in surgery. In the 22 patients of group A, the proximal fixed vertebral lamina and PLC were not resected, and in the 49 patients of group B, the proximal fixed vertebral lamina and PLC were resected completely. Age, sex, body mass index (BMI), number of fixed vertebrae and fused levels, spinopelvic parameters, coronal Cobb angle, and modified Pfirrmann grading system were measured for each patient. A Cox proportional hazards model was used to analyze risk factors for upper ASD. No symptomatic ASD was found during the follow-up period. Patients who underwent proximal fixed vertebral lamina and PLC resection had a significantly higher percentage of radiographic ASD (P = 0.042). The Cox proportional hazards model showed that age, sex, BMI, preoperative lumbar lordosis, sacral slope, pelvic tilt, coronal Cobb angle, number of fixed vertebrae, and interbody fusion levels had no significant differences for radiographic ASD. But a preoperative modified Pfirrmann grade higher than 3, a high degree of preoperative pelvic incidence, and more decompressed levels had statistical significance (P = 0.024, 0.041, and 0.008, respectively). A preoperative modified Pfirrmann grade higher than 3, a high degree of preoperative pelvic incidence, and more decompressed levels might be risk factors for upper radiographic ASD after multi-level posterior lumbar spinal fusion surgery.