Ighmbp2 基因突变与疾病病理:确定区分 SMARD1 和 CMT2S 的差异。

IF 4.6 2区 医学 Q1 NEUROSCIENCES Experimental Neurology Pub Date : 2024-10-24 DOI:10.1016/j.expneurol.2024.115025
Sara M. Ricardez Hernandez , Bassil Ahmed , Yaser Al Rawi , F. Javier Llorente Torres , Mona O. Garro Kacher , Catherine L. Smith , Zayd Al Rawi , Jessica Garcia , Nicole L. Nichols , Christian L. Lorson , Monique A. Lorson
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引用次数: 0

摘要

免疫球蛋白μDNA结合蛋白2(IGHMBP2)基因突变会导致两种不同的疾病,即SMA伴呼吸窘迫I型(SMARD1)和Charcot玛丽齿2S型(CMT2S)。为了了解 SMARD1 和 CMT2S 的表型和分子差异,以及 IGHMBP2 在疾病发展中的作用,我们根据六例 IGHMBP2 患者的突变生成了小鼠模型。此前,我们报道了 Ighmbp2D564N/D564N 小鼠的开发和特征描述,在本手稿中,我们研究了两种突变:在本手稿中,我们研究了 Ighmbp2H922Y/H922Y 和 Ighmbp2D564N/H922Y 上下文中的 D565N(小鼠为 D564N)和 H924Y(小鼠为 H922Y)。我们发现这些小鼠模型之间存在明显差异,这为我们深入了解 IGHMBP2 在 SMARD1 和 CMT2S 发病机制中的作用提供了重要依据。重要的是,这些研究还证明了在 Ighmbp2 D564N 和 H922Y 同源隐性突变和复合杂合突变的情况下,疾病的发病机制是如何发生显著改变的。值得注意的是,在 Ighmbp2 D564N/H922Y 小鼠中存在短寿命和长寿命群组,早期(P12/P16)呼吸系统病理变化是预测寿命的关键因素。尽管寿命存在差异,但所有 Ighmbp2D564N/H922Y 小鼠的运动功能缺陷都很早就开始出现,并逐渐恶化。Ighmbp2D564N/H922Y小鼠的肢体骨骼肌纤维面积减少,神经肌肉接头(NMJ)去神经化增加。与 CMT2S 相一致,Ighmbp2H922Y/H922Y 小鼠的寿命和呼吸系统病理学均无改变。有趣的是,Ighmbp2H922Y/H922Y 四肢肌肉纤维显示出肌肉纤维面积先增加后减少,而 NMJ 神经支配的变化即使在 180 岁时也很小。这是第一项证明 IGHMBP2 呼吸功能与四肢运动功能存在差异的研究。对于我们了解 IGHMBP2 的功能具有重要意义的是,我们证明了与这些 IGHMBP2 患者突变相关的疾病发病机制与 IGHMBP2 的生化活性之间存在直接关联。重要的是,这些研究揭示了细胞内存在单个突变蛋白(IGHMBP2-D564N 或 IGHMBP2-H922Y)或两个突变蛋白(IGHMBP2-D564N 和 IGHMBP2-H922Y)时的动态差异。
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Ighmbp2 mutations and disease pathology: Defining differences that differentiate SMARD1 and CMT2S
Mutations in the Immunoglobulin mu DNA binding protein 2 (IGHMBP2) gene result in two distinct diseases, SMA with Respiratory Distress Type I (SMARD1) and Charcot Marie Tooth Type 2S (CMT2S). To understand the phenotypic and molecular differences between SMARD1 and CMT2S, and the role of IGHMBP2 in disease development, we generated mouse models based on six IGHMBP2 patient mutations. Previously, we reported the development and characterization of Ighmbp2D564N/D564N mice and in this manuscript, we examine two mutations: D565N (D564N in mice) and H924Y (H922Y in mice) in the Ighmbp2H922Y/H922Y and Ighmbp2D564N/H922Y contexts. We found significant differences between these mouse models, providing critical insight into the role of IGHMBP2 in the pathogenesis of SMARD1 and CMT2S. Importantly, these studies also demonstrate how disease pathogenesis is significantly altered in the context of Ighmbp2 D564N and H922Y homozygous recessive and compound heterozygous mutations. Notably, there were short-lived and long-lived lifespan cohorts within Ighmbp2D564N/H922Y mice with early (P12/P16) respiratory pathology serving as a key predictor of lifespan. Despite differences in lifespan, motor function deficits initiated early and progressively worsened in all Ighmbp2D564N/H922Y mice. There was decreased limb skeletal muscle fiber area and increased neuromuscular junction (NMJ) denervation in Ighmbp2D564N/H922Y mice. Consistent with CMT2S, Ighmbp2H922Y/H922Y mice did not have altered lifespans nor respiratory pathology. Interestingly, Ighmbp2H922Y/H922Y limb muscle fibers demonstrated an increase in muscle fiber area followed by a reduction while changes in NMJ innervation were minimal even at P180. This is the first study that demonstrates differences associated with IGHMBP2 function within respiration with those within limb motor function. Significant to our understanding of IGHMBP2 function, we demonstrate that there is a direct correlation between disease pathogenesis associated with these IGHMBP2 patient mutations and IGHMBP2 biochemical activity. Importantly, these studies reveal the dynamic differences that are presented when either a single mutant protein is present (IGHMBP2-D564N or IGHMBP2-H922Y) or two mutant proteins are present (IGHMBP2-D564N and IGHMBP2-H922Y) within cells.
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来源期刊
Experimental Neurology
Experimental Neurology 医学-神经科学
CiteScore
10.10
自引率
3.80%
发文量
258
审稿时长
42 days
期刊介绍: Experimental Neurology, a Journal of Neuroscience Research, publishes original research in neuroscience with a particular emphasis on novel findings in neural development, regeneration, plasticity and transplantation. The journal has focused on research concerning basic mechanisms underlying neurological disorders.
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