白细胞介素-1β诱导人椎间盘退变中的血管生成和神经支配。

Interleukin-1β induces angiogenesis and innervation in human intervertebral disc degeneration.

机构信息

Department of Orthopaedic Surgery, CHA Bundang Medical Center, CHA University, Gyeonggi-do 463-712, Korea.

出版信息

J Orthop Res. 2011 Feb;29(2):265-9. doi: 10.1002/jor.21210.

Abstract

Degenerative disorders of the intervertebral discs (IVDs) are generally characterized by enhanced matrix degradation, angiogenesis, innervation, and increased expression of catabolic cytokines. In this study, we investigated the effects of inflammatory cytokines, IL-1β, and TNF-α, on the expression of an angiogenic factor, vascular endothelial growth factor (VEGF), and neurotrophic factors, nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF), in human IVD degeneration. IL-1β and TNF-α stimulated the gene expression of VEGF, NGF, and BDNF in nucleus pulposus (NP) cells isolated from patient tissues. Immunohistochemical results demonstrated a positive correlation between IL-1β and VEGF/NGF/BDNF expression in human IVD tissues. RNA expression analysis of patient tissues also identified positive correlations between VEGF and platelet endothelial cell adhesion molecule-1 (PECAM-1) and between NGF/BDNF and protein gene product 9.5 (PGP9.5). Our findings suggest that IL-1β is generated during IVD degeneration, which stimulates the expression of VEGF, NGF, and BDNF, resulting in angiogenesis and innervation.

摘要

椎间盘(IVD)退行性疾病的特征通常为基质降解、血管生成、神经支配增强以及分解代谢细胞因子表达增加。在这项研究中,我们研究了炎症细胞因子 IL-1β 和 TNF-α 对人 IVD 退变中血管生成因子血管内皮生长因子(VEGF)和神经营养因子神经生长因子(NGF)和脑源性神经营养因子(BDNF)表达的影响。IL-1β 和 TNF-α 刺激从患者组织中分离的髓核(NP)细胞中 VEGF、NGF 和 BDNF 的基因表达。免疫组织化学结果表明,人 IVD 组织中 IL-1β 与 VEGF/NGF/BDNF 表达之间存在正相关。对患者组织的 RNA 表达分析还确定了 VEGF 与血小板内皮细胞黏附分子-1(PECAM-1)之间以及 NGF/BDNF 与蛋白基因产物 9.5(PGP9.5)之间存在正相关。我们的研究结果表明,IL-1β 在 IVD 退变过程中产生,刺激 VEGF、NGF 和 BDNF 的表达,从而导致血管生成和神经支配。

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