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轻度肌病与 COMP 相关,但与遗传骨骼疾病的小鼠模型中的 MATN3 突变无关。

Mild myopathy is associated with COMP but not MATN3 mutations in mouse models of genetic skeletal diseases.

机构信息

Institute of Genetic Medicine, Newcastle University, Newcastle upon Tyne, United Kingdom.

出版信息

PLoS One. 2013 Nov 27;8(11):e82412. doi: 10.1371/journal.pone.0082412. eCollection 2013.

Abstract

Pseudoachondroplasia (PSACH) and multiple epiphyseal dysplasia (MED) are skeletal disorders resulting from mutations in COMP, matrilin-3 or collagen IX and are characterised by short-limbed dwarfism and premature osteoarthritis. Interestingly, recent reports suggest patients can also manifest with muscle weakness. Here we present a detailed analysis of two mouse models of the PSACH/MED disease spectrum; ΔD469 T3-COMP (PSACH) and V194D matrilin-3 (MED). In grip test experiments T3-COMP mice were weaker than wild-type littermates, whereas V194D mice behaved as controls, confirming that short-limbed dwarfism alone does not contribute to PSACH/MED-related muscle weakness. Muscles from T3-COMP mice showed an increase in centronuclear fibers at the myotendinous junction. T3-COMP tendons became more lax in cyclic testing and showed thicker collagen fibers when compared with wild-type tissue; matrilin-3 mutant tissues were indistinguishable from controls. This comprehensive study of the myopathy associated with PSACH/MED mutations enables a better understanding of the disease progression, confirms that it is genotype specific and that the limb weakness originates from muscle and tendon pathology rather than short-limbed dwarfism itself. Since some patients are primarily diagnosed with neuromuscular symptoms, this study will facilitate better awareness of the differential diagnoses that might be associated with the PSACH/MED spectrum and subsequent care of PSACH/MED patients.

摘要

假性软骨发育不全症(PSACH)和多发性骨骺发育不良症(MED)是由 COMP、软骨寡聚基质蛋白-3 或胶原 IX 基因突变引起的骨骼疾病,其特征为短肢侏儒症和骨关节炎。有趣的是,最近的报告表明,患者也可能表现出肌肉无力。在这里,我们对 PSACH/MED 疾病谱的两种小鼠模型进行了详细分析;ΔD469 T3-COMP(PSACH)和 V194D 软骨寡聚基质蛋白-3(MED)。在握力测试实验中,T3-COMP 小鼠比野生型同窝仔鼠弱,而 V194D 小鼠的行为与对照鼠相同,这证实了单纯的短肢侏儒症并不导致 PSACH/MED 相关的肌肉无力。T3-COMP 小鼠的肌肉在肌肌腱交界处出现中心核纤维增加。与野生型组织相比,T3-COMP 肌腱在循环测试中变得更加松弛,并且胶原纤维更厚;软骨寡聚基质蛋白-3 突变组织与对照组织没有区别。这项对与 PSACH/MED 突变相关的肌病的综合研究使我们能够更好地理解疾病进展,证实它是特定于基因型的,并且肢体无力源自肌肉和肌腱病理,而不是短肢侏儒症本身。由于一些患者主要被诊断为神经肌肉症状,因此这项研究将有助于更好地了解可能与 PSACH/MED 谱相关的鉴别诊断,并为 PSACH/MED 患者提供后续护理。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/367b/3842254/e63f410d0cc4/pone.0082412.g001.jpg

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