PDF(Pubmed)
Abstract：
BACKGROUND: Human intervertebral disk degeneration (IVDD) is a sophisticated degenerative pathological process. A key cause of IVDD progression is nucleus pulposus cell (NPC) degeneration, which contributes to excessive endoplasmic reticulum stress in the intervertebral disk. However, the mechanisms underlying IVDD and NPC degeneration remain unclear.
METHODS: We used interleukin (IL)-1β stimulation to establish an NPC-degenerated IVDD model and investigated whether human urine-derived stem cell (USC) exosomes could prevent IL-1β-induced NPC degeneration using western blotting, quantitative real-time polymerase chain reaction, flow cytometry, and transcriptome sequencing techniques.
RESULTS: We successfully extracted and identified USCs and exosomes from human urine. IL-1β substantially downregulated NPC viability and induced NPC degeneration while modulating the expression of SOX-9, collagen II, and aggrecan. Exosomes from USCs could rescue IL-1β-induced NPC degeneration and restore the expression levels of SOX-9, collagen II, and aggrecan.
CONCLUSIONS: USC-derived exosomes can prevent NPCs from degeneration following IL-1β stimulation. This finding can aid the development of a potential treatment strategy for IVDD.
METHODS: We used interleukin (IL)-1β stimulation to establish an NPC-degenerated IVDD model and investigated whether human urine-derived stem cell (USC) exosomes could prevent IL-1β-induced NPC degeneration using western blotting, quantitative real-time polymerase chain reaction, flow cytometry, and transcriptome sequencing techniques.
RESULTS: We successfully extracted and identified USCs and exosomes from human urine. IL-1β substantially downregulated NPC viability and induced NPC degeneration while modulating the expression of SOX-9, collagen II, and aggrecan. Exosomes from USCs could rescue IL-1β-induced NPC degeneration and restore the expression levels of SOX-9, collagen II, and aggrecan.
CONCLUSIONS: USC-derived exosomes can prevent NPCs from degeneration following IL-1β stimulation. This finding can aid the development of a potential treatment strategy for IVDD.
摘要：
背景：人椎间盘退变（IVDD）是一种复杂的退行性病理过程。IVDD进展的关键原因是髓核细胞（NPC）变性，这有助于椎间盘内质网过度应激。然而,IVDD和NPC变性的潜在机制尚不清楚.
方法：我们使用白细胞介素（IL）-1β刺激建立NPC退化的IVDD模型，并使用蛋白质印迹法研究人尿源干细胞（USC）外泌体是否可以预防IL-1β诱导的NPC变性，定量实时聚合酶链反应，流式细胞术,和转录组测序技术。
结果：我们成功地从人尿液中提取并鉴定了USCs和外泌体。IL-1β显著下调NPC活力并诱导NPC变性，同时调节SOX-9，胶原II的表达，和aggrecan。来自USCs的外泌体可以挽救IL-1β诱导的NPC变性并恢复SOX-9，胶原蛋白II的表达水平，和aggrecan。
结论：USC衍生的外泌体可以防止IL-1β刺激后NPC变性。这一发现可以帮助开发IVDD的潜在治疗策略。
方法：我们使用白细胞介素（IL）-1β刺激建立NPC退化的IVDD模型，并使用蛋白质印迹法研究人尿源干细胞（USC）外泌体是否可以预防IL-1β诱导的NPC变性，定量实时聚合酶链反应，流式细胞术,和转录组测序技术。
结果：我们成功地从人尿液中提取并鉴定了USCs和外泌体。IL-1β显著下调NPC活力并诱导NPC变性，同时调节SOX-9，胶原II的表达，和aggrecan。来自USCs的外泌体可以挽救IL-1β诱导的NPC变性并恢复SOX-9，胶原蛋白II的表达水平，和aggrecan。
结论：USC衍生的外泌体可以防止IL-1β刺激后NPC变性。这一发现可以帮助开发IVDD的潜在治疗策略。
