Mariano Jennifer M, Joca Humberto C, Kallenbach Jacob, Ranu Natasha, Ochala Julien, Ward Christopher, Kontrogianni-Konstantopoulos Aikaterini
Department of Biochemistry and Molecular Biology and.
Department of Orthopaedics, University of Maryland School of Medicine, Baltimore, Maryland, USA.
JCI Insight. 2025 Jun 26;10(15). doi: 10.1172/jci.insight.182471. eCollection 2025 Aug 8.
Dominant missense mutations in MYBPC1, the gene encoding the essential sarcomeric slow Myosin Binding Protein-C (sMyBP-C), are associated with Myotrem, a new, early-onset congenital myopathy characterized by muscle weakness, hypotonia, skeletal deformities, and myogenic tremor. Importantly, the clinical manifestation of Myotrem in mid- and late adulthood is unknown. Using the Myotrem MYBPC1 E248K-knock-in (E248K-KI) murine model, we interrogated contractile performance of soleus, gastrocnemius, and tibalis anterior (TA) muscles in both male and female mice in mid- (12 months) and late (24 months) adulthood. Our findings show that the phenotypic manifestation of E248K Myotrem differs across muscle type, sex, and age. While KI soleus muscle consistently exhibited contractile impairment across both sexes and ages, KI gastrocnemius muscle displayed preserved force production. Interestingly, TA muscle showed a sex- and age-specific effect with preserved function through 12 months in both sexes and a sharp decline at 24 months solely in males. Quantitative analysis of TA sarcomeric organization uncovered structural deficits coinciding with contractile dysfunction, supporting the notion that sMyBP-C serves a primarily structural role in skeletal muscle. Collectively, our studies reveal that aging affects the E248K Myotrem myopathy in a muscle- and sex-dependent fashion and show that sarcomeric disorganization accompanies contractile deterioration in affected muscles.
肌小节必需的慢肌球蛋白结合蛋白C(sMyBP-C)的编码基因MYBPC1中的显性错义突变与肌阵挛有关,肌阵挛是一种新的早发性先天性肌病,其特征为肌肉无力、肌张力减退、骨骼畸形和肌源性震颤。重要的是,肌阵挛在成年中期和晚期的临床表现尚不清楚。利用肌阵挛MYBPC1 E248K敲入(E248K-KI)小鼠模型,我们研究了成年中期(12个月)和晚期(24个月)雄性和雌性小鼠比目鱼肌、腓肠肌和胫骨前肌(TA)的收缩性能。我们的研究结果表明,E248K肌阵挛的表型表现因肌肉类型、性别和年龄而异。虽然KI比目鱼肌在两性和各年龄段均持续表现出收缩功能受损,但KI腓肠肌的力量产生保持正常。有趣的是,TA肌表现出性别和年龄特异性效应,在12个月时两性的功能均保持正常,而仅在24个月大的雄性小鼠中出现急剧下降。对TA肌小节组织的定量分析发现,结构缺陷与收缩功能障碍同时出现,支持了sMyBP-C在骨骼肌中主要起结构作用的观点。总的来说,我们的研究表明,衰老以肌肉和性别依赖的方式影响E248K肌阵挛性肌病,并表明肌小节紊乱伴随着受影响肌肉的收缩功能恶化。