MicroRNA dysregulation in ataxia telangiectasia

Front Immunol. 2024 Aug 19:15:1444130. doi: 10.3389/fimmu.2024.1444130. eCollection 2024.

Abstract

Introduction: Ataxia telangiectasia (AT) is a rare disorder characterized by neurodegeneration, combined immunodeficiency, a predisposition to malignancies, and high clinical variability. Profiling of microRNAs (miRNAs) may offer insights into the underlying mechanisms of complex rare human diseases, as miRNAs play a role in various biological functions including proliferation, differentiation, and DNA repair. In this study, we investigate the differential expression of miRNAs in samples from AT patients to identify miRNA patterns and analyze how these patterns are related to the disease.

Methods: We enrolled 20 AT patients (mean age 17.7 ± 9.6 years old) and collected clinical and genetic data. We performed short non-coding RNA-seq analysis on peripheral blood mononuclear cells (PBMCs) and fibroblasts to compare the miRNA expression profile between AT patients and controls.

Results: We observed 42 differentially expressed (DE)-miRNAs in blood samples and 26 in fibroblast samples. Among these, three DE-miRNAs, miR-342-3p, miR-30a-5p, and miR-195-5p, were further validated in additional AT samples, confirming their dysregulation.

Discussion: We identified an AT-related miRNA signature in blood cells and fibroblast samples collected from a group of AT patients. We also predicted several dysregulated pathways, primarily related to cancer, immune system control, or inflammatory processes. The findings suggest that miRNAs may provide insights into the pathophysiology and tumorigenesis of AT and have the potential to serve as useful biomarkers in cancer research.

Keywords: DNA repair; ataxia telangiectasia; cancer; immunodeficiency; microRNA.

MeSH terms

  • Adolescent
  • Adult
  • Ataxia Telangiectasia* / genetics
  • Child
  • Female
  • Fibroblasts / metabolism
  • Gene Expression Profiling
  • Gene Expression Regulation
  • Humans
  • Leukocytes, Mononuclear* / metabolism
  • Male
  • MicroRNAs* / blood
  • MicroRNAs* / genetics
  • Young Adult

Substances

  • MicroRNAs

Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This work was supported by Ricerca Finalizzata 2016, Ministero della Salute public Grant (2016-02364303) and partially by the Associazione Nazionale Atassia Telangiectasia (ANAT) “Milestone Research Grant,” European Union-Next Generation EU-PNRR M6C2-Investimento 2.1 Valorizzazione e potenziamento della Ricerca Biomedica del SSN (PNRR–MR1–2022–12376594), Bando Ricerca Finalizzata Ministero della Salute 2019 (RF-2019–12369979), and Bando PRIN (2022ZCLC3X). Some authors are part of the European Reference Network on Rare Primary Immunodeficiency, Autoinflammatory and Autoimmune Diseases (ERN-RITA)–Project ID no. 739543.