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Single-cell transcriptomics reveals keratinocyte dynamic processes associated with S100a4 expression in psoriasiform

Huiqin Wang1,2,3, Yuan Ding1,2,3, Shirong Yu1,2,3

  • 1Department of Dermatology and Venereology, People's Hospital of Xinjiang Uygur Autonomous Region, Urumqi, China.

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The study shows that removing the S100A4 gene improves psoriasis-like skin conditions in mice by reducing inflammation and epidermal thickening. This suggests S100A4 plays a role in psoriasis development and offers potential therapeutic targets.

Keywords:
S100a4 knockoutimmune regulationkeratinocytespsoriasissingle-cell RNA sequencing

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Area of Science:

  • Dermatology
  • Immunology
  • Molecular Biology

Background:

  • Psoriasis is an autoimmune skin disease characterized by epidermal hyperplasia and immune cell infiltration.
  • S100A4, an antimicrobial peptide, is highly expressed in psoriatic skin, but its function remains unclear.

Purpose of the Study:

  • To investigate the role of S100A4 in psoriasis pathogenesis.
  • To elucidate the molecular mechanisms underlying S100A4's function in skin inflammation.

Main Methods:

  • Generated S100a4 gene knockout mice using CRISPR/Cas9.
  • Induced psoriasis-like lesions using imiquimod.
  • Analyzed epidermal cell composition and gene expression via single-cell RNA sequencing (scRNA-seq) and bioinformatics.

Main Results:

  • S100a4 knockout mice showed reduced inflammation and epidermal hyperplasia.
  • scRNA-seq revealed decreased pathogenic keratinocytes and downregulated TNF and IL-17 signaling.
  • S100A4 depletion normalized keratinocyte proliferation and differentiation, restoring homeostasis.

Conclusions:

  • S100A4 plays a pathogenic role in psoriasis.
  • Findings reveal novel cell-specific regulatory mechanisms in psoriasis.
  • S100A4 may be a therapeutic target for psoriasis treatment.