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Long-term exposure of human endothelial cells to metformin modulates miRNAs and isomiRs

Angelica Giuliani1, Eric Londin2, Manuela Ferracin3

  • 1Department of Clinical and Molecular Sciences, Università Politecnica Delle Marche, Via Tronto 10/A, 60126, Ancona, Italy.

Scientific Reports
|December 14, 2020
PubMed

Insights

Metformin, a diabetes drug, alters microRNA (miRNA) and microRNA isoform (isomiR) patterns in aging human endothelial cells. This reshaping of miRNA/isomiR profiles offers new insights into cellular senescence.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Gerontology

Background:

  • Metformin, a widely used glucose-lowering medication, is increasingly recognized for its anti-senescence properties.
  • Emerging research suggests metformin influences microRNA (miRNA) biogenesis.
  • MicroRNA isoforms (isomiRs) represent sequence variations of canonical miRNAs, potentially altering their function.

Purpose of the Study:

  • To comprehensively analyze the impact of metformin on miRNA and isomiR profiles in human endothelial cells experiencing replicative senescence.
  • To investigate how metformin modulates the expression and relative abundance of specific miRNAs and their isoforms during cellular aging.

Main Methods:

  • Analysis of miRNA and isomiR profiles in human endothelial cells treated with metformin during replicative senescence.
  • Differential expression analysis of miRNAs and isomiRs.
  • Pathway enrichment analysis to identify biological processes affected by metformin-regulated miRNAs and isomiRs.

Main Results:

  • Metformin treatment led to differential expression of 27 miRNAs, including notable examples like miR-100-5p and miR-217.
  • IsomiR analysis revealed that non-canonical sequences constitute a significant portion (nearly 40%) of the miRNA pool.
  • Metformin significantly altered the relative abundance of 133 isomiRs, including non-canonical forms of key miRNAs. Some isomiRs exhibited alternative seed sequences and distinct target profiles compared to canonical forms.
  • Pathway analysis indicated that metformin modulates pathways related to proliferation and nutrient sensing via regulated miRNAs.

Conclusions:

  • Metformin significantly reshapes the senescence-associated miRNA and isomiR landscape in endothelial cells.
  • The study expands the understanding of the molecular mechanisms underlying metformin's anti-senescence effects.
  • The findings highlight the importance of considering isomiRs in miRNA-mediated drug actions and cellular processes like senescence.

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