银屑病
透皮
角质层
角质形成细胞
免疫系统
伊米奎莫德
药理学
间充质干细胞
细胞因子
全身给药
TLR7型
小干扰RNA
化学
前蛋白转化酶
肿瘤坏死因子α
癌症研究
细胞生长
炎症
医学
细胞
串扰
细胞培养
免疫学
伤口愈合
作者
Hanxue Zhou,Jiaye Lu,Bei Yin,Yu Meng,Congcong Zhu,Xiying Wu,Jun Liu,Quangang Zhu,Zongguang Tai,Zhongjian Chen
标识
DOI:10.1002/adhm.202504232
摘要
Psoriasis onset is closely associated with abnormal lipid metabolism. Proprotein convertase subtilisin/kexin type 9 (PCSK9), a pivotal regulator of lipid metabolism, has recently been implicated in keratinocyte hyperproliferation and immune dysregulation in psoriasis.However, transdermal delivery of siRNAs forPCSK9 inhibition is challenging.To address this limitation, we developed a dissolvable microneedle (MN) platform encapsulating mesenchymal stem cell (MSC)-derived biomimetic nanovesicles (MSCNV) loaded with siPCSK9 (MN-MSCNV@siPCSK9). This integrated platform facilitates stabilized siRNA encapsulation via MSCNV-mediated protection, enables efficient transdermal delivery via stratum corneum disruption, and leverages MSCNV's inherent bioactivity for synergistic immunomodulation. In vitro, MN-MSCNV@siPCSK9 significantly inhibited keratinocyte proliferation and pro-inflammatory cytokine secretion. In vivo, it alleviated imiquimod (IMQ)-induced psoriasis symptoms by reducing epidermal hyperplasia and systemic inflammation. Mechanistically, the platform suppressed nuclear factor-kappa B (NF-κB) pathway activation, modulated Th1, Th2, and Th17 cell subsets, and disrupted the inflammatory crosstalk between keratinocytes and immune cells. Consequently, it coordinately regulates both local and systemic inflammatory microenvironments. This study establishes a translatable "encapsulation-delivery-modulation" strategy, providing a potent gene-silencing platform for precision psoriasis therapy.
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