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Quantitative Proteomics Identifies Reduced NRF2 Activity and Mitochondrial Dysfunction in Atopic Dermatitis.

Michael Koch1, Tobias Kockmann2, Elke Rodriguez3

  • 1Institute of Molecular Health Sciences, Department of Biology, ETH Zürich, Zürich, Switzerland.

The Journal of Investigative Dermatology
|September 15, 2022
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Summary

This study reveals key proteomic changes in atopic dermatitis (AD) epidermis, highlighting impaired keratinocyte differentiation and the NRF2-antioxidant pathway. These findings offer insights into AD pathogenesis and potential therapeutic targets.

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Area of Science:

  • Dermatology
  • Proteomics
  • Molecular Biology

Background:

  • Atopic dermatitis (AD) is a common inflammatory skin condition with a compromised epidermal barrier.
  • Keratinocyte dysfunction is implicated in AD, but comprehensive epidermal proteomic changes remain unclear.

Purpose of the Study:

  • To define the full epidermal proteome alterations in atopic dermatitis.
  • To investigate the role of keratinocytes and the NRF2-antioxidant pathway in AD pathogenesis.

Main Methods:

  • Quantitative proteomics using pressure-cycling technology and data-independent acquisition on human epidermis (healthy, lesional AD, nonlesional AD).
  • Validation via targeted proteomics (parallel reaction monitoring mass spectrometry) and immunofluorescence staining.
  • siRNA-mediated NRF2 knockdown in primary human keratinocytes.

Main Results:

  • Identified differentially abundant proteins in AD epidermis, reflecting inflammation and impaired keratinocyte differentiation/stratification.
  • Revealed impaired NRF2-antioxidant pathway activation and reduced mitochondrial protein abundance in lesional AD skin.
  • Demonstrated a partial interlink between impaired NRF2 activation and mitochondrial abnormalities in keratinocytes.

Conclusions:

  • Epidermal proteomic alterations in AD include inflammation, differentiation defects, and mitochondrial dysfunction.
  • Impaired NRF2-antioxidant pathway and mitochondrial issues are interconnected in AD epidermis.
  • Findings suggest novel therapeutic targets for atopic dermatitis treatment.