Identification of shared pathogenic signatures of multiple sclerosis and chronic obstructive pulmonary disease: an

Arman Mokaram Doust Delkhah1

  • 1Department of Cell and Molecular Biology, Faculty of Life Sciences and Biotechnology, Shahid Beheshti University, Tehran, Iran. arman.mokaram@gmail.com.

PubMed

Insights

Patients with multiple sclerosis (MS) and chronic obstructive pulmonary disease (COPD) share molecular links. Peripheral blood leukocytes may bridge these conditions, with TP53 and specific microRNAs identified as key players.

Area of Science:

  • Immunology
  • Genomics
  • Pulmonology

Background:

  • Multiple sclerosis (MS) patients have an increased risk of developing chronic obstructive pulmonary disease (COPD).
  • The underlying molecular mechanisms connecting MS and COPD remain largely unidentified.
  • Peripheral blood leukocytes are emerging as a potential link between autoimmune disorders and COPD.

Purpose of the Study:

  • To identify shared molecular signatures between MS and COPD using blood transcriptome data.
  • To explore the role of peripheral blood leukocytes in the co-occurrence of MS and COPD.
  • To uncover potential therapeutic targets by analyzing shared gene expression patterns.

Main Methods:

  • Gene expression datasets for MS and COPD were retrieved from the Gene Expression Omnibus (GEO) database.
  • Differentially expressed genes (DEGs) were identified for each disease.
  • A protein-protein interaction (PPI) network was constructed for shared DEGs to identify hub genes and regulatory microRNAs (miRNAs).

Main Results:

  • A total of 246 genes showed consistent expression changes in both MS and COPD.
  • A PPI network revealed TP53, H4C6, SNRPE, and RPS11 as key hub genes.
  • Eight miRNAs were identified as key regulators, including miR-218-5p and miR-142-5p, suggesting an epigenetic link.

Conclusions:

  • Peripheral blood leukocytes may act as a bridge connecting the pathogenesis of MS and COPD.
  • Shared molecular signatures, including specific genes and miRNAs, offer insights into the link between these conditions.
  • TP53, miR-218-5p, and miR-142-5p are potential key players requiring further investigation for therapeutic development.