Psoriasis-susceptibility-related RNA gene induced by stress (PRINS) (PRINS)

Psoriasis-susceptibility-related RNA gene induced by stress (PRINS) is a primate-specific long non-coding RNA (lncRNA) that plays a pivotal role in the regulation of keratinocyte stress responses and the pathogenesis of psoriasis. It was originally identified as one of the most highly expressed transcripts in the non-lesional epidermis of psoriasis patients, suggesting it serves as a susceptibility factor or a modifier of the disease phenotype. Biologically, PRINS functions by interacting with the nucleophosmin (NPM1) protein and regulating the expression of the anti-apoptotic gene G1P3 (IFI6), thereby protecting skin cells from environmental stressors like UV radiation or serum starvation. In psoriatic skin, the elevated levels of PRINS in non-lesional areas may predispose keratinocytes to abnormal inflammatory responses, while its relatively lower levels in active lesions suggest a complex role in disease maintenance. PRINS also demonstrates anti-inflammatory properties by modulating the expression of key cytokines, including IL-6, CCL-5, and IL-23, which are central to the psoriatic inflammatory cascade. Although no therapeutic agents currently target PRINS directly in clinical practice, its role as a regulatory hub in epidermal homeostasis makes it a potential target for future RNA-based therapies. Research into PRINS has also extended to other conditions, such as diabetic nephropathy, where it interacts with the Smad7 signaling pathway.

Other names

Psoriasis-associated RNA induced by non-specific stimuliPsoriasis-associated non-protein coding RNA induced by stressPRINS lncRNAPsoriasis susceptibility-related RNA gene induced by stress

PRINS acts as a regulatory long non-coding RNA that modulates the cellular stress response and apoptosis in keratinocytes by interacting with the nucleophosmin (NPM1) protein and regulating the expression of the anti-apoptotic gene G1P3 (also known as IFI6). It also influences the production of pro-inflammatory cytokines such as IL-6, CCL-5, and IL-23 by modulating their mRNA stability or signaling pathways.