
Effects of Autophagy Modulators and Dioxin on the Expression of Epidermal Differentiation Proteins on Psoriasis-Like Keratinocytes in vitro and ex vivo
Author(s) -
Hye Ran Kim,
Hye One Kim,
Jin Cheol Kim,
Chun Wook Park,
Bo Young Chung
Publication year - 2022
Publication title -
clinical, cosmetic and investigational dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 35
ISSN - 1178-7015
DOI - 10.2147/ccid.s368105
Subject(s) - hacat , psoriasis , keratinocyte , downregulation and upregulation , aryl hydrocarbon receptor , autophagy , ex vivo , chemistry , epidermis (zoology) , cancer research , in vivo , microbiology and biotechnology , biology , immunology , in vitro , apoptosis , transcription factor , biochemistry , anatomy , gene
Psoriasis is a chronic inflammatory skin disorder associated with impairment of epidermal differentiation. Many signaling pathways, including those involved in aryl hydrocarbon receptor (AHR) and autophagy dysfunction, are reportedly associated with the pathogenesis of psoriasis. However, the discrete effects of dioxin via AHR activation or autophagy on the epidermal barrier remain unclear. In the current study, we evaluated the effects of autophagy modulators (chloroquine [CQ] and rapamycin) and the AHR agonist TCDD on the expression of epidermal barrier proteins in psoriasis-like keratinocytes and psoriasis lesional skin tissue culture.