ArticleImmunity, inflammation and disease2026
Adiponectin Inhibits AURKA to Suppress Inflammation in TNF-α-induced Keratinocytes and Attenuates Psoriatic Dermatitis in Mice.
Article in Immunity, inflammation and disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Adiponectin Inhibits AURKA to Suppress Inflammation in TNF-α-induced Keratinocytes and Attenuates Psoriatic Dermatitis in Mice.Immunity, inflammation and disease · 2026Article
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6 authors.
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Abstract
introductionPsoriasis is a recurrent immune-mediated systemic disease. Adiponectin (APN), a key regulator of metabolism, is also known for its anti-inflammatory properties in several inflammatory disorders. The study aims to investigate the anti-inflammatory properties of APN on human immortalized keratinocyte cells (HaCaT) and to evaluate its therapeutic potential in an imiquimod (IMQ)-induced psoriasis mouse model.
methodsHaCaT cells were treated with 5, 10, or 20 μg/ml APN, and cell viability was assessed. A psoriasis-like cellular model was created by exposing HaCaT cells to TNF-α (50 ng/ml) for a duration of 24 h. Apoptosis was analyzed using flow cytometry, and the secretion of inflammatory cytokines was measured through enzyme-linked immunosorbent assay (ELISA). Real-time quantitative polymerase chain reaction (RT-qPCR) was used to measure the mRNA expression levels of AdipoR1, AdipoR2, and T-cadherin(T-cad). Aurora kinase A (AURKA) and Forkhead transcription factor 1 (FOXM1) were analyzed using Western blotting (WB) and RT-qPCR. The anti-psoriatic effect of APN was also evaluated in IMQ-induced psoriatic dermatitis. Additionally, ELISA and WB were used to assess cytokines and key signaling proteins in mouse skin tissues.
resultsAPN significantly inhibited the proliferation of HaCaT cells and enhanced their apoptosis. Additionally, it decreased the production of interleukin (IL)-1β, IL-8, and IL-6. APN upregulated AdipoR1 and AdipoR2 mRNA levels while downregulating the mRNA and protein levels of T-cad. Mechanistically, APN mitigated the inflammatory response in keratinocytes by suppressing the TNF-α-induced upregulation of AURKA and FOXM1. This mechanism was substantiated in vivo, where APN treatment alleviated IMQ-induced psoriatic dermatitis in mice, concurrently reducing levels of IL-1β, CXCL2 and IL-6, and modulating the expression of AdipoR1, AdipoR2, AURKA, and FOXM1 in mouse skin.
conclusionOur findings suggest that APN inhibits keratinocyte hyperproliferation and suppresses inflammation in TNF-α-induced keratinocytes. Moreover, APN treatment attenuates IMQ-induced psoriatic dermatitis in mice, supporting its potential as a therapeutic approach for psoriasis.
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