S100A4在银屑病炎症中的机制研究  

Mechanism Study of S100A4 in Psoriasis Inflammation

作　　者：李响 吴卫东[2] 

机构地区：[1]石河子大学医学院,新疆 石河子 [2]新疆维吾尔自治区人民医院皮肤性病科,新疆 乌鲁木齐

出　　处：《临床医学进展》2024年第3期855-861,共7页Advances in Clinical Medicine

摘　　要：目的:探究S100钙结合蛋白A4 (S100 Calcium Binding Protein A4, S100A4)在银屑病炎症中的作用机制。方法:在HaCat细胞中使用S100A4的抗体进行改进的紫外交联免疫共沉淀结合高通量测序(improved RNA Binding Protein Immunoprecipitation high throughput sequencing, iRIP-seq)技术获得与S100A4互作的RNA,将相关基因序列比对KEGG数据库来明确S100A4调控的炎症通路。结果:S100A4结合的靶RNA所在基因与MAPK信号通路、核糖体、内质网中的蛋白质加工、糖尿病并发症中的AGE-RAGE信号通路、膀胱癌、慢性髓样白血病、弓形体病、结肠直肠癌、破骨细胞分化、军团杆菌病等功能通路的调节有关,表明S100A4可能是调节银屑病及其并发症的一种关键炎症介质。结论:S100A4在银屑病炎症机制中具有潜在的调控作用,这些发现为S100A4作为银屑病发病炎症介质提供了新的证据。Objective: Explore the mechanism of S100 calcium binding protein A4 in psoriasis inflammation. Methods: Improved RNA Binding Protein Immunoprecipitation high throughput sequencing using S100A4 antibodies in HaCat cells was used to obtain RNA that interacts with S100A4. The relevant gene sequences were aligned with the KEGG database to identify the inflammatory pathway regu-lated by S100A4. Results: The target RNA of S100A4 is related to MAPK signaling pathway, ribo-some, protein processing in the endoplasmic reticulum, AGE-RAGE signaling pathway in diabetic complications, bladder cancer, chronic myeloid leukemia, toxoplasmosis, colorectal cancer, osteo-clast differentiation, and legionellosis, indicating that S100A4 may be a key inflammatory mediator regulating psoriasis and its complications. Conclusion: S100A4 has a potential regulatory role in the inflammatory mechanism of psoriasis, and these findings provide new evidence for S100A4 as an inflammatory mediator in the pathogenesis of psoriasis.

关 键 词：S100A4 银屑病 炎症 

分 类 号：R75[医药卫生—皮肤病学与性病学]