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Related Experiment Video

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Loricrin and NRF2 Coordinate Cornification.

Yosuke Ishitsuka1, Tatsuya Ogawa2, Yoshiyuki Nakamura2

  • 1Department of Dermatology, Graduate School of Medicine, Osaka University, Osaka, Japan.

JID Innovations : Skin Science From Molecules to Population Health
|January 13, 2022
PubMed
Summary
This summary is machine-generated.

Loricrin knockout mice show impaired skin barrier repair. Antioxidant responses compensate for defects, highlighting loricrin and NRF2

Keywords:
CD, corneodesmosomeCDSN, corneodesmosinCE, cornified envelopeCEf, immature/fragile cornified envelopeDKO, Lor–Nrf2 double knockoutDMF, dimethyl fumarateK, keratinKC, keratinocyteLG, lamellar granuleLKO, Lor knockoutLOR, loricrinNKO, Nrf2 knockoutSC, stratum corneumSG, stratum granulosumTEWL, transepidermal water lossTS, tape-strippingWT, wild type

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Area of Science:

  • Dermatology
  • Cell Biology
  • Biochemistry

Background:

  • Cornification forms the skin's protective barrier via corneocytes and intercellular lipids.
  • Loricrin is crucial for structural integrity, but its necessity for desiccation resistance is debated.
  • KEAP1/NRF2 pathway activation may compensate for loricrin deficiency during development.

Purpose of the Study:

  • Investigate postnatal skin barrier function in loricrin knockout (LKO) mice.
  • Determine how compensatory responses are activated after initial defects are repaired.
  • Clarify the roles of loricrin and NRF2 in epidermal barrier maintenance and repair.

Main Methods:

  • Postnatal phenotyping of LKO mice.
  • Ultrastructural analysis of epidermal barrier components.
  • Assessment of permeability barrier function.
  • Gene expression analysis related to epidermal repair pathways.

Main Results:

  • LKO mice exhibit thinner cornified cell envelopes and more lamellar granules.
  • Superficial skin damage triggers NRF2-dependent repair mechanisms.
  • Impaired degradation of corneodesmosomes observed in LKO mice.
  • Enhanced lamellar granule secretion in response to epidermal damage.

Conclusions:

  • Loricrin and NRF2 are key regulators of cornification and skin barrier function.
  • The skin barrier actively repairs itself through coordinated protein secretion, cross-linking, and degradation.
  • NRF2-mediated responses are critical for compensating structural defects in loricrin deficiency.