Adiponectin Upregulates Filaggrin Expression via SIRT1-Mediated Signaling in Human Normal Keratinocytes.
- Author:
Taewon JIN
1
;
Kui Young PARK
;
Seong Jun SEO
Author Information
- Publication Type:Original Article
- Keywords: Adiponectin; ARNT; Filaggrin; Keratinocytes; SIRT1
- MeSH: Adiponectin*; Amino Acids; Aryl Hydrocarbon Receptor Nuclear Translocator; Cytoskeleton; Down-Regulation; Humans*; Keratinocytes*; Permeability; RNA, Small Interfering; Seizures; Signal Transduction; Skin; Water
- From:Annals of Dermatology 2017;29(4):407-413
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND: Filaggrin (FLG) is the major component of the epidermal granular layer and binds to and condenses the keratin cytoskeleton. FLG thus contributes to cell compaction and serves as a natural moisturizing factor by promoting unfolding and degradation into hygroscopic amino acids. Loss or downregulation of FLG has been shown to result in a weak stratum corneum, which causes water loss and increases the possibility of skin barrier-related seizure. Adiponectin (Acrp30) contributes to the functional recovery of somatic cells, including human normal epidermal keratinocytes (NHEKs). OBJECTIVE: To investigate the effect of Acrp30 in FLG expression and identifying its signal transduction mechanism. METHODS: Normal human keratinocytes were treated with Acrp30 and the levels of FLG were examined. Silent mating type information regulation 2 homolog (SIRT)-targeting siRNA and aryl hydrocarbon receptor nuclear translocator (ARNT)-targeting siRNA were used to identify the role of various signal transduction pathway components. RESULTS: Acrp30 upregulated SIRT1 and ARNT expression in NHEKs, resulting in increased FLG expression. Treatment with both SIRT1-targeting siRNA and ARNT-targeting siRNA blocked Acrp30 stimulation and silenced FLG expression. CONCLUSION: Adiponectin upregulates FLG expression through a SIRT1-mediated pathway. Our results suggest that Acrp30 is a promising agent for skin barrier permeability improvement.