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SPNS1 deficiency alleviates the development of atopic dermatitis by suppressing keratinocyte proliferation
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DOI：10.2306/scienceasia1513-1874.2026.035.png)
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Abstract
En 中文
This study aimed to investigate the role of the protein SPNS1 in the pathogenesis of atopic dermatitis (AD) and the underlying mechanisms, with a particular focus on keratinocyte proliferation and lysosomal function. Analysis of GEO datasets revealed a significant upregulation of SPNS1 in lesional skin from AD patients and DNCB-induced mouse models. An AD-like mouse model was established by applying DNCB to SPNS1 heterozygous (SPNS1+/-) mice, and human keratinocytes (HaCaT) were stimulated with IL-4/IL-13 following SPNS1 knockdown. Epidermal thickness and cell proliferation were assessed via H&E staining and Ki-67 immunofluorescence, while cell viability, apoptosis, and lysosomal morphology were evaluated using the CCK-8 assay, flow cytometry, and immunofluorescence, respectively. The results showed that SPNS1 deficiency alleviated AD-like skin inflammation and epidermal hyperplasia. Both in vivo and in vitro, SPNS1 knockdown suppressed keratinocyte hyperproliferation, induced G1/S cell cycle arrest, and promoted apoptosis. Moreover, SPNS1 deficiency disrupted lysosomal morphology and function. Clinically, effective AD treatment was associated with downregulated SPNS1 expression. These findings demonstrate that SPNS1 promotes AD progression by driving keratinocyte hyperproliferation, potentially through the disruption of lysosomal homeostasis, thereby positioning SPNS1 as a promising therapeutic target for AD.
Keywords:
atopic dermatitis
SPNS1
keratinocytes
cell proliferation
apoptosis
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