A Sex-Specific Anti-Inflammatory Role for p62 in Psoriasis-Like Disease
Psoriasis is a chronic inflammatory skin disease involving a complex cross-talk between immune and epidermal cells. Psoriasis is difficult to treat and often complicated by systemic manifestations such as psoriatic arthritis. SQSTM1/p62 is a multifunctional adaptor protein controlling autophagy, cell differentiation, and inflammation that was found elevated in human psoriatic skin. We functionally evaluated the role of p62 in the cutaneous and systemic psoriasis-like phenotypes of a mouse model with inducible epidermal inactivation of c-Jun and JunB (ie, DKO∗). A male-specific aggravation of skin and joint disease was observed in DKO∗ mice when crossed with p62<sup>-/-</sup> mice (DKO∗ p62<sup>-/-</sup>). Thickened epidermis, disturbed keratinocyte differentiation, enhanced immune cell infiltration, and increased CXCL1 expression were exclusively observed in the skin of male DKO∗ p62<sup>-/-</sup> mice. Increased androgen receptor protein expression and activation of androgen receptor signaling as well as upregulated inflammasome and KEAP1/NRF2 activities were apparent in the skin of male DKO∗ p62<sup>-/-</sup> mice and were likely responsible for disease worsening. Our results describe a sex-specific anti-inflammatory role for p62 in psoriasis-like disease that could be relevant in the clinical setting.
Authors
- Johannes Griss (ORCID: https://orcid.org/0000-0003-2206-9511)
- Erwin F. Wagner (ORCID: https://orcid.org/0000-0001-7872-0196)
- K. Mieczkowski
- Latifa Bakiri (ORCID: https://orcid.org/0000-0002-6300-2420)
Institutions
- Medical University of Vienna (AT)
Publication Details
- Journal
- Journal of Investigative Dermatology
- Published
- 2025-04-19
- DOI
- https://doi.org/10.1016/j.jid.2025.04.004
- Citations
- 3
- Primary Topic
- Psoriasis: Treatment and Pathogenesis
- Type
- article
- Field-Weighted Citation Impact
- 2.39
Funders
- Austrian Science Fund
- Medizinische Universität Wien
- Horizon 2020 Framework Programme
- European Research Council
- H2020 Marie Skłodowska-Curie Actions