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Stage-dependent transcriptomic changes in human dermal fibroblast senescence model.

Michiko Kudo1,2, Ryo Yonezawa1, Hideaki Mizobata1

  • 1Laboratory of Aquatic Molecular Biology and Biotechnology, Department of Aquatic Bioscience, Graduate School of Agricultural and Life Science, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo, 113-8657 Japan.

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Summary
This summary is machine-generated.

Cellular senescence involves distinct gene expression changes as cells age. Immune responses activate early, while structural maintenance declines progressively, offering new therapeutic targets for aging.

Keywords:
aging biomarkerscellular senescencedermal fibroblastsimmune–inflammatory signalingtranscriptome analysis

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Area of Science:

  • Cellular biology
  • Aging research
  • Genomics

Background:

  • Cellular senescence is crucial in aging and age-related diseases.
  • The precise gene expression dynamics during senescence are not fully understood.

Purpose of the Study:

  • To investigate gene expression changes throughout aging progression.
  • To identify molecular mechanisms driving senescence.
  • To explore potential biomarkers and therapeutic targets for aging.

Main Methods:

  • Utilized three replicative senescence models of human dermal fibroblasts (young, middle, old).
  • Performed RNA sequencing transcriptome analysis with two analytical pipelines.
  • Conducted differential expression analysis, STRING, Gene Ontology/Kyoto Encyclopedia of Genes and Genomes enrichment, and non-negative matrix factorization (NMF).

Main Results:

  • Transcriptome profiles differed significantly between young/middle and old stages.
  • Gene expression changes (differentially expressed genes) increased with senescence progression.
  • Early activation of immune-inflammatory responses and decreased structural maintenance genes were observed.
  • NMF confirmed immune-inflammatory activation and loss of structural maintenance functions.

Conclusions:

  • Immune-inflammatory responses are activated early in senescence.
  • Cell adhesion and maintenance pathways decline progressively during aging.
  • Identified early biomarkers and therapeutic targets to potentially mitigate aging-related functional decline.