Dataset Information

Proteomics of Human Skeletal Muscle

ABSTRACT: The skeletal muscle proteomics study of vastus lateralis muscle biopsies which were collected from participants from the Genetic and Epigenetic Study of Aging and Laboratory Testing (GESTALT). The participants were free of major diseases, except for controlled hypertension or a history of cancer that had been clinically silent for at least 10 years, were not chronically medicated (except one on antihypertensive medication), had no physical or cognitive impairments, had a BMI less than 30 kg/m2, and were not professional athletes.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (ncbitaxon:9606)

SUBMITTER: Luigi Ferrucci

PROVIDER: MSV000096122 | MassIVE | Thu Oct 17 19:55:00 BST 2024

SECONDARY ACCESSION(S): PXD011967

REPOSITORIES: MassIVE

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Publications

Discovery proteomics in aging human skeletal muscle finds change in spliceosome, immunity, proteostasis and mitochondria.

Ubaida-Mohien Ceereena C Lyashkov Alexey A Gonzalez-Freire Marta M Tharakan Ravi R Shardell Michelle M Moaddel Ruin R Semba Richard D RD Chia Chee W CW Gorospe Myriam M Sen Ranjan R Ferrucci Luigi L

eLife 20191023

A decline of skeletal muscle strength with aging is a primary cause of mobility loss and frailty in older persons, but the molecular mechanisms of such decline are not understood. Here, we performed quantitative proteomic analysis from skeletal muscle collected from 58 healthy persons aged 20 to 87 years. In muscle from older persons, ribosomal proteins and proteins related to energetic metabolism, including those related to the TCA cycle, mitochondria respiration, and glycolysis, were underrepr ...[more]

PMID: 31642809

Publication: 1/2

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Project description:Preclinical models of type 1 diabetes mellitus exhibit marked declines in skeletal muscle health including significant impairments in muscle repair. The present study investigated, for the first time, whether muscle repair was altered in young adults with uncomplicated type 1 diabetes (T1D) following damaging exercise.In this cohort study, eighteen physically-active young adults (M=22.1, SEM=0.9 years) with T1D (n, male/female=4/5; MHbA1c= 58, SEMHbA1c=5.9 mmol/mol) and without T1D (n, male/female=4/5) performed 300 unilateral eccentric contractions (90°s-1) of the knee extensors. Prior to exercise, at 48-hours and at 96-hours after exercise, participants gave a venous blood sample and vastus lateralis biopsy and performed a maximal voluntary isometric knee extension. Skeletal muscle extracellular matrix content, and satellite cell content/proliferation were assessed by immunofluorescence. Transmission electron microscopy was used to quantify ultrastructural damage.Maximal isometric strength was comparable between T1D and their sex-matched control group prior to exercise for both sexes. Immediately following damaging exercise, strength was decreased in both groups but there was a moderate effect size for lower strength during recovery in the T1D group at both 48-hours and 96-hours. Serum creatine kinase, an indicator of muscle damage, was moderately higher in T1D participants compared to controls at rest, and exhibited a small elevation 96-hours after exercise. Immunofluorescence analyses showed satellite cell content was lower at all timepoints in those with type 1 diabetes. T1D participants demonstrated a moderate delay in satellite cell proliferation (as assessed by Pax7+/Ki67+ nuclei counts) after exercise, reaching peak levels of proliferation 48-hours after control participants. Despite these differences, those with T1D did not exhibit greater ultrastructural muscle damage than controls as assessed by electron microscopy. Finally, a transcriptomic investigation of T1D muscle revealed several networks of dysregulated genes involving RNA translation as well as mitochondrial respiration function, providing potential explanations for previous observations of mitochondrial dysfunction in similar T1D cohorts. Our novel findings indicate that skeletal muscle from physically active, young adults with moderately controlled T1D may have a reduced ability to handle, and repair from, damaging exercise. While larger cohort studies are clearly needed, these results suggest that those with T1D may require longer recovery times following damaging exercise.