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首页> 外文期刊>Journal of orthopaedic research >Canonical Wnt signaling in the notochordal cell is upregulated in early intervertebral disk degeneration
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Canonical Wnt signaling in the notochordal cell is upregulated in early intervertebral disk degeneration

机译：早期椎间盘退变中脊索细胞中的典型Wnt信号上调

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摘要

The notochordal cell (NC) of the nucleus pulposus (NP) is considered a potential NP progenitor cell, and early intervertebral disk (IVD) degeneration involves replacement of NCs by chondrocyte-like cells (CLCs). Wnt/β-catenin signaling plays a crucial role in maintaining the notochordal fate during embryogenesis, but is also involved in tissue degeneration and regeneration. The canine species, which can be subdivided into non-chondrodystrophic and chondrodystrophic breeds, is characterized by differential maintenance of the NC: in non-chondrodystrophic dogs, the NC remains the predominant cell type during the majority of life, with IVD degeneration only occurring at old age; conversely, in chondrodystrophic dogs the NC is lost early in life, with concurrent degeneration of all IVDs. This study investigated Wnt/β-catenin signaling in the healthy, NC-rich NP and early degenerated, CLC-rich NP of both breed types by immunohistochemistry of β-catenin and relative gene expression of brachyury and cytokeratin 8 (notochordal markers) and Wnt targets axin2, cyclin D1, and c-myc. Both NCs and CLCs showed nuclear and cytoplasmic β-catenin protein expression and axin2 gene expression, but β-catenin signal intensity and Wnt target gene expression were higher in the CLC-rich NP. Primary NCs in monolayer culture (normoxic conditions) showed Wnt/β-catenin signaling comparable to the in vivo situation, with increased cyclin D1 and c-myc gene expression. In conclusion, Wnt/β-catenin signaling activity in the NC within the NC-rich NP and in culture supports the role of this cell as a potential progenitor cell; increased Wnt/β-catenin signaling activity in early IVD degeneration may be a reflection of its dual role.
机译：髓核（NP）的脊索细胞（NC）被认为是潜在的NP祖细胞，并且早期椎间盘（IVD）变性涉及用类软骨细胞（CLC）替代NC。 Wnt /β-catenin信号传导在维持胚胎发生过程中的脊索命运中起着至关重要的作用，但也参与组织变性和再生。犬种可细分为非软骨营养不良和软骨营养不良的品种，其特征在于NC的差异性维持：在非软骨营养不良的犬种中，NC仍然是生命中主要的细胞类型，IVD变性仅发生在老年;相反，在软骨营养不良的犬中，NC会在生命的早期丢失，同时导致所有IVD退化。本研究通过β-catenin的免疫组织化学以及近距离吸血和细胞角蛋白8（脊索标记）和Wnt的相对基因表达，研究了两种类型的健康，富含NC的NP和早期变性，富含CLC的NP中的Wnt /β-catenin信号传导靶向axin2，cyclin D1和c-myc。 NCs和CLCs均显示核和细胞质β-catenin蛋白表达和axin2基因表达，但β-catenin信号强度和Wnt靶基因表达在富含CLC的NP中较高。单层培养（常氧条件下）的原发性NCs表现出与体内情况相当的Wnt /β-catenin信号传导，细胞周期蛋白D1和c-myc基因表达增加。总之，Wnt /β-catenin信号传导在富含NC的NP内的NC中以及在培养物中均支持该细胞作为潜在祖细胞的作用。早期IVD变性中Wnt /β-catenin信号传导活性的增加可能是其双重作用的反映。

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