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FMyBP-C is a vital regulator in young and aged fast skeletal muscle homeostasis

ABSTRACT: Skeletal Myosin binding protein-C (MyBP-C) paralogs, slow (sMyBP-C) and fast (fMyBP-C) interacts with myosin and actin filaments within sarcomeres, modulating the force development during contraction. These display differential expression in muscle fibres, with fMyBP-C higher in fast twitch fibres. However, our knowledge about the changes in the fMyBP-C expression in diseased conditions and its role in skeletal muscle aging is lacking. In this study we use mice model lacking fMyBP-C to understand its significance in skeletal muscle physiology. Skeletal muscle samples from wild type and Mybpc2 knockout (C2-/-)old male mice (22 months) were used to define the role of fMyBP-C in aging. Western immunoblotting was employed to analyze the expression of fMyBP-C and sMyBP-C, and phosphorylation status of sMyBP-C. The impact of C2-/- and aging on the fiber type, size, and number as well as general muscle structure was assessed by immunohistochemistry and electron microscopy. The functional effect of C2-/- and aging was measured in terms of in vivo and ex vivo muscle force generation. Lastly, RNA sequencing was performed to identify the molecular pathways dysregulated in the C2-/- mediated muscle dysfunction in young and old mice. The aged male C2-/- mice compared to their wildtype counterparts, display significant deficits in muscle strength and endurance, accompanied by changes in muscle fiber size and molecular signaling pathways critical for muscle homeostasis.Thus, fMyBP-C is an important regulator of muscle function and homeostasis in the young and aged fast-twitch muscle fibers. The absence of fMyBP-C aggravates the effect of aging on muscle structure and function. fMyBP-C has the potential to be a therapeutic target to modulate muscle wasting caused by aging and disease.

ORGANISM(S): Mus musculus

PROVIDER: GSE285405 | GEO | 2025/12/04

REPOSITORIES: GEO

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Project description:This a model from the article: A mathematical model of fatigue in skeletal muscle force contraction. Shorten PR, O'Callaghan P, Davidson JB, Soboleva TK. J Muscle Res Cell Motil 2007;28(6):293-313 18080210 , Abstract: The ability for muscle to repeatedly generate force is limited by fatigue. The cellular mechanisms behind muscle fatigue are complex and potentially include breakdown at many points along the excitation-contraction pathway. In this paper we construct a mathematical model of the skeletal muscle excitation-contraction pathway based on the cellular biochemical events that link excitation to contraction. The model includes descriptions of membrane voltage, calcium cycling and crossbridge dynamics and was parameterised and validated using the response characteristics of mouse skeletal muscle to a range of electrical stimuli. This model was used to uncover the complexities of skeletal muscle fatigue. We also parameterised our model to describe force kinetics in fast and slow twitch fibre types, which have a number of biochemical and biophysical differences. How these differences interact to generate different force/fatigue responses in fast- and slow- twitch fibres is not well understood and we used our modelling approach to bring new insights to this relationship. This model was taken from the CellML repository and automatically converted to SBML. The original model was: Shorten PR, O'Callaghan P, Davidson JB, Soboleva TK. (2007) - version02 This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information. In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not.. To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.

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FMyBP-C is a vital regulator in young and aged fast skeletal muscle homeostasis

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