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首页> 外文期刊>Journal of cellular physiology. >Absence of VEGFR-1/Flt-1 signaling pathway in mice results in insensitivity to discogenic low back pain in an established disc injury mouse model
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Absence of VEGFR-1/Flt-1 signaling pathway in mice results in insensitivity to discogenic low back pain in an established disc injury mouse model

机译：在老鼠身上缺乏VEGFR-1 / Flt-1信号通路导致discogenic下腰上的疏忽疼痛椎间盘损伤小鼠模型建立

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Although degenerative disc disease (DDD) and related low back pain (LBP) are growing public health problems, the underlying disease mechanisms remain unclear. An increase in the vascular endothelial growth factor (VEGF) levels in DDD has been reported. This study aimed to examine the role of VEGF receptors (VEGFRs) in DDD, using a mouse model of DDD. Progressive DDD was induced by anterior stabbing of lumbar intervertebral discs in wild type (WT) and VEGFR-1 tyrosine-kinase deficient mice (vegfr-1~(TK-/-)). Pain assessments were performed weekly for 12 weeks. Histological and immunohistochemical assessments were made for discs, dorsal root ganglions, and spinal cord. Both vegfr-1~(TK-/-) and WT mice presented with similar pathological changes in discs with an increased expression of inflammatory cytokines and matrix-degrading enzymes. Despite the similar pathological patterns, vegfr-1~(TK-/-) mice showed insensitivity to pain compared with WT mice. This insensitivity to discogenic pain was related to lower levels of pain factors in the discs and peripheral sensory neurons and lower spinal glial activation in the vegfr-1~(TK-/-) mice than in the WT mice. Exogenous stimulation of bovine disc cells with VEGF increased inflammatory and cartilage degrading enzyme. Silencing vegfr-1 by small-interfering-RNA decreased VEGF-induced expression of pain markers, while silencing vegfr-2 decreased VEGF-induced expression of inflammatory and metabolic markers without changing pain markers. This suggests the involvement of VEGFR-1 signaling specifically in pain transmission. Collectively, our results indicate that the VEGF signaling is involved in DDD. Particularly, VEGFR-1 is critical for discogenic LBP transmission independent of the degree of disc pathology.
机译：尽管(DDD)和退行性椎间盘疾病相关下腰痛(LBP)的增长健康问题,潜在的疾病机制尚不清楚。血管内皮生长因子(VEGF)水平DDD的报道。检查(VEGFRs) VEGF受体的作用DDD,使用鼠标的DDD模式。是引起腰椎前刺在野生型(WT)和椎间盘VEGFR-1酪氨酸-缺陷小鼠(vegfr-1 ~ (TK - / -))。每周进行12周。免疫组织化学进行了评估光盘、背根神经节和脊髓。vegfr-1 ~ (TK - / -)和WT老鼠了相似的病理变化与一个光盘增加炎症细胞因子的表达和基质降解酶。病理模式,vegfr-1 ~ (TK - / -)小鼠显示与WT相比对疼痛的不敏感老鼠。相关的疼痛程度较低的因素光盘和周边感觉神经元和低脊髓胶质激活vegfr-1 ~ (TK - / -)老鼠比WT老鼠。牛椎间盘细胞的VEGF增加炎症和软骨降解酶。沉默vegfr-1由small-interfering-RNA减少VEGF-induced痛苦的表情标记,而沉默vegfr-2下降VEGF-induced炎症和的表情代谢标记不改变痛苦标记。这表明VEGFR-1的参与专在痛苦中传输信号。总的来说,我们的结果表明,VEGF信号是参与DDD。VEGFR-1 discogenic枸杞多糖是至关重要的传输的独立程度的圆盘病理

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