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SM/J 小鼠的椎间盘早期退变与离子转运系统的变化和纤维化事件有关。

Early onset of disc degeneration in SM/J mice is associated with changes in ion transport systems and fibrotic events.

机构信息

School of Biomedical Sciences, The University of Hong Kong, Pokfulam, Hong Kong SAR, China.

Centre for Genomic Sciences, The University of Hong Kong, Pokfulam, Hong Kong SAR, China.

出版信息

Matrix Biol. 2018 Sep;70:123-139. doi: 10.1016/j.matbio.2018.03.024. Epub 2018 Apr 9.

Abstract

Intervertebral disc degeneration (IDD) causes back pain and sciatica, affecting quality of life and resulting in high economic/social burden. The etiology of IDD is not well understood. Along with aging and environmental factors, genetic factors also influence the onset, progression and severity of IDD. Genetic studies of risk factors for IDD using human cohorts are limited by small sample size and low statistical power. Animal models amenable to genetic and functional studies of IDD provide desirable alternatives. Despite differences in size and cellular content as compared to human intervertebral discs (IVDs), the mouse is a powerful model for genetics and assessment of cellular changes relevant to human biology. Here, we provide evidence for early onset disc degeneration in SM/J relative to LG/J mice with poor and good tissue healing capacity respectively. In the first few months of life, LG/J mice maintain a relatively constant pool of notochordal-like cells in the nucleus pulposus (NP) of the IVD. In contrast, chondrogenic events are observed in SM/J mice beginning as early as one-week-old, with progressive fibrotic changes. Further, the extracellular matrix changes in the NP are consistent with IVD degeneration. Leveraging on the genomic data of two parental and two recombinant inbred lines, we assessed the genetic contribution to the NP changes and identified processes linked to the regulation of ion transport systems. Significantly, "transport" system is also in the top three gene ontology (GO) terms from a comparative proteomic analysis of the mouse NP. These findings support the potential of the SM/J, LG/J and their recombinant inbred lines for future genetic and biological analysis in mice and validation of candidate genes and biological relevance in human cohort studies. The proteomic data has been deposited to the ProteomeXchange Consortium via the PRIDE [1] partner repository with the dataset identifier PXD008784.

摘要

椎间盘退变(IDD)导致背痛和坐骨神经痛,影响生活质量,造成高经济/社会负担。IDD 的病因尚不清楚。除了年龄和环境因素外,遗传因素也会影响 IDD 的发病、进展和严重程度。使用人类队列进行 IDD 危险因素的遗传研究受到样本量小和统计效力低的限制。可进行遗传和功能研究的动物模型为 IDD 提供了理想的替代方法。尽管大小和细胞含量与人类椎间盘(IVD)不同,但小鼠是研究遗传学和评估与人类生物学相关的细胞变化的有力模型。在这里,我们提供了证据证明 SM/J 相对于 LG/J 小鼠的椎间盘退变发病更早,而 LG/J 小鼠具有良好的组织愈合能力。在生命的头几个月,LG/J 小鼠在 IVD 的髓核(NP)中保持相对恒定的脊索样细胞池。相比之下,早在一周大时就可以观察到 SM/J 小鼠的软骨形成事件,并且会逐渐出现纤维化变化。此外,NP 中的细胞外基质变化与 IVD 退变一致。利用两个亲本和两个重组近交系的基因组数据,我们评估了 NP 变化的遗传贡献,并确定了与离子转运系统调节相关的过程。重要的是,“运输”系统也是对小鼠 NP 进行比较蛋白质组学分析的前三个基因本体论(GO)术语之一。这些发现支持 SM/J、LG/J 及其重组近交系在未来的遗传和生物学分析中的潜力,以及在人类队列研究中验证候选基因和生物学相关性。蛋白质组学数据已通过 PRIDE [1] 合作伙伴存储库存入 ProteomeXchange 联盟,数据集标识符为 PXD008784。

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