AI Article Synopsis

  • The study investigates long non-coding RNAs (lncRNAs) and their roles in sustaining dystrophin protein stability and influencing muscle cell growth and development, focusing on Duchenne muscular dystrophy (DMD) using DMD/mdx mouse models.
  • A total of 554 differentially expressed lncRNAs were identified, with 373 upregulated and 181 downregulated, some of which have potential regulatory roles in crucial genes connected to DMD.
  • The research utilized various tools to predict the regulatory networks involving lncRNAs, miRNAs, and mRNAs, revealing that certain lncRNAs could indirectly regulate important genes associated with DMD, opening new avenues for therapies.

Article Abstract

This study explored the significance of long non-coding RNAs (lncRNAs), particularly their role in maintaining dystrophin protein stability and regulating myocyte proliferation and differentiation. The investigation focused on DMD/mdx mouse skeletal muscle primary myoblasts, aiming to identify lncRNAs potential as biomarkers and therapeutic targets for Duchenne muscular dystrophy (DMD). Utilizing CLC Genomics Workbench software, 554 differentially expressed lncRNAs were identified in DMD/mdx mice compared to wild-type (WT) control. Among them, 373 were upregulated, and 181 were downregulated. The study highlighted specific lncRNAs (e.g., 5930430L01Rik, Gm10143, LncRNA1490, LncRNA580) and their potential regulatory roles in DMD key genes like IGF1, FN1, TNNI1, and MYOD1. By predicting miRNA and their connections with lncRNA and mRNA (ceRNA network) using tools such as miRNet, miRSYSTEM and miRCARTA, the study revealed potential indirect regulation of Dystrophin, IGF1R and UTRN genes by identified lncRNAs (e.g. 2310001H17Rik-203, C130073E24Rik-202, LncRNA2767, 5930430L01Rik and LncRNA580). These findings suggest that the identified lncRNAs may play crucial roles in the development and progression of DMD through their regulatory influence on key gene expression, providing valuable insights for potential therapeutic interventions.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11467414PMC
http://dx.doi.org/10.1038/s41598-024-75221-7DOI Listing

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