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Updated: Aug 6, 2026

Generation and Culturing of Primary Human Keratinocytes from Adult Skin
Published on: December 22, 2017
N-acetyltransferase 10 regulates chemokine expression in keratinocytes and promotes atopic dermatitis
Jinjin Shao1, Linying Wang2, Zhichao Ye2
1Zhejiang Key Laboratory of High-level Biosafety and Biomedical Transformation, Hangzhou Medical College, Hangzhou, China; Key Laboratory of Drug Safety Evaluation and Research of Zhejiang Province, Center of Safety Evaluation and Research, Hangzhou Medical College, Hangzhou, China.
Abstract:
Atopic dermatitis (AD) is a chronic relapsing inflammatory skin disorder with complex immunological underpinnings, yet the role of the RNA acetyltransferase NAT10 in its pathogenesis remains unclear. We investigated NAT10 function through cutaneous NAT10 knockdown (microneedle-delivered AAV-shRNA) and pharmacological inhibition (Remodelin), using 2,4-dinitrochlorobenzene- and ovalbumin-induced murine AD models combined with IFN-γ/TNF-α-stimulated HaCaT keratinocytes. Results showed elevated NAT10 expression and acetylcytidine modification in AD keratinocytes. NAT10 knockdown ameliorated skin pathology, reduced serum IgE, and selectively limited neutrophil infiltration by suppressing chemokines (CXCL8, CCL5, CXCL9, CXCL10, CCL2), whereas its overexpression promoted their expression. Mechanistically, NAT10 stabilized RELB mRNA via acetylcytidine modification, thereby activating NF-κB signaling. Remodelin suppressed keratinocyte chemokine production and neutrophil recruitment, improving skin lesions without toxicity. Collectively, NAT10 emerges as a central regulator of keratinocyte-driven inflammation and a viable therapeutic target in AD.
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