AI Article Synopsis

  • - The study investigates how tRNA-derived fragments, specifically mt-Ty 5' tiRNAs, influence gene expression in skeletal muscle cell growth and development.
  • - Techniques like Northern blotting, RT-PCR, and RNA-Seq were used to analyze the impact of altering mt-Ty 5' tiRNA levels on muscle cell proliferation and differentiation.
  • - Findings revealed that lower levels of mt-Ty 5' tiRNAs hinder muscle cell growth and development, while increasing these fragments promotes healthier muscle cell function, suggesting their potential as new targets for treating muscle diseases.

Article Abstract

In this study, we sought to determine the role of tRNA-derived fragments in the regulation of gene expression during skeletal muscle cell proliferation and differentiation. We employed cell culture to examine the function of mt-Ty 5' tiRNAs. Northern blotting, RT-PCR as well as RNA-Seq, were performed to determine the effects of mt-Ty 5' tiRNA loss and gain on gene expression. Standard and transmission electron microscopy (TEM) were used to characterize cell and sub-cellular structures. mt-Ty 5'tiRNAs were found to be enriched in mouse skeletal muscle, showing increased levels in later developmental stages. Gapmer-mediated inhibition of tiRNAs in skeletal muscle C2C12 myoblasts resulted in decreased cell proliferation and myogenic differentiation; consistent with this observation, RNA-Seq, transcriptome analyses, and RT-PCR revealed that skeletal muscle cell differentiation and cell proliferation pathways were also downregulated. Conversely, overexpression of mt-Ty 5'tiRNAs in C2C12 cells led to a reversal of these transcriptional trends. These data reveal that mt-Ty 5'tiRNAs are enriched in skeletal muscle and play an important role in myoblast proliferation and differentiation. Our study also highlights the potential for the development of tiRNAs as novel therapeutic targets for muscle-related diseases.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10392060PMC
http://dx.doi.org/10.1111/cpr.13416DOI Listing

Publication Analysis

Top Keywords

skeletal muscle
24
cell proliferation
16
muscle cell
12
proliferation differentiation
12
mt-ty 5'tirnas
12
differentiation study
8
gene expression
8
5'tirnas enriched
8
cell
7
mt-ty
6

Similar Publications

Physical activity, cathepsin B, and cognitive health.

Trends Mol Med

January 2025

Body-Brain-Mind Laboratory, School of Psychology, Shenzhen University, Shenzhen, 518060, China. Electronic address:

Regular physical activity (PA) is beneficial for cognitive health, and cathepsin B (CTSB) - a protease released by skeletal muscle during PA - acts as a potential molecular mediator of this association. PA-induced metabolic and mechanical stress appears to increase plasma/serum CTSB levels. CTSB facilitates neurogenesis and synaptic plasticity in brain regions (e.

View Article and Find Full Text PDF

Homozygous missense variant in causes early-onset neurodegeneration, leukoencephalopathy and autoinflammation.

J Med Genet

January 2025

Division of Clinical and Metabolic Genetics, Department of Paediatrics, The Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada

Biallelic pathogenic variants in cause a fatal autosomal recessive multisystem disorder characterized by recurrent autoinflammation, hypomyelination, progressive neurodegeneration, microcephaly, failure to thrive, liver dysfunction, respiratory chain defects and accumulation of glycogen in skeletal muscle. No missense variants in have been reported to date.We report a 6-year-old boy with microcephaly, global developmental delays, lower limb spasticity with hyperreflexia, epilepsy, abnormal brain MRI, failure to thrive, recurrent fevers and transaminitis.

View Article and Find Full Text PDF

Skeletal muscle disorders as risk factors for type 2 diabetes.

Mol Cell Endocrinol

January 2025

Department of Physiology and Biophysics, Rush University, Chicago, United States.

The incidence and prevalence of muscular disorders and of type 2 diabetes (T2D) is increasing and both represent highly significant healthcare problems, both economically and compromising quality of life. Interestingly, skeletal muscle dysfunction and T2D share some commonalities including dysregulated glucose homeostasis, increased oxidative stress, dyslipidemia, and cytokine alterations. Several lines of evidence have hinted to a relationship between skeletal muscle dysfunction and T2D.

View Article and Find Full Text PDF

Gut Microbiota-Bone Axis.

Ann Nutr Metab

January 2025

Department of Translational Medical Science, University of Naples Federico II, Napoli, Italy.

Background: Knowledge of the complex interplay between gut microbiota and human health is gradually increasing as it has just recently been a field of such great interest.

Summary: Recent studies have reported that communities of microorganisms inhabiting the gut influence the immune system through cellular responses and shape many physiological and pathophysiological aspects of the body, including muscle and bone metabolism (formation and resorption). Specifically, the gut microbiota affects skeletal homeostasis through changes in host metabolism, the immune system, hormone secretion, and the gut-brain axis.

View Article and Find Full Text PDF

Objective: This study aimed to explore the predictive value of baseline CT body composition and its early changes on recurrence-free survival (RFS) following radical gastrectomy, while also assessing potential sex-related differences.

Methods: We conducted a retrospective analysis of gastric cancer (GC) patients with confirmed pathology from October 2019 to May 2023. All patients underwent preoperative and postoperative CT scans to assess visceral fat area (VFA), subcutaneous fat area (SFA), skeletal muscle area (SMA), and skeletal muscle density (SMD), along with calculating their respective rates of change.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!