加勒-3/CD146相互作用促进损伤和急性损伤后的全身炎症
L Boutin1,2,3, S M Figueroa3, E Roger3
1Department of Anesthesia and Critical Care, Hôpital Européen Georges Pompidou (HEGP), Leblanc, Paris, France.
Scientific reports
|November 25, 2025
概括
加勒-3 (Gal-3) 通过激活内皮细胞,促进缺血后的损伤. 阻断Gal-3可减少急性损伤 (AKI) 模型中的炎症和损伤.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學專業.
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
背景情况:
- 加勒-3 (Gal-3) 表达增加了后缺血性损伤,导致组织损伤.
- 在急性损伤 (AKI) 期间,Gal-3在内皮激活和炎症中的作用尚不清楚.
研究的目的:
- 调查Gal-3在AKI中对内皮激活和炎症的作用机制.
- 确定3-表达在组织与全身循环对AKI结果的影响.
主要方法:
- 使用野生型和Gal-3淘汰赛小鼠进行缺血-再输液 (rIR).
- 使用骨髓移植来区分Gal-3表达源.
- 通过免疫光,西部斑点和scRNAseq.评估Gal-3表达.
- 使用等离子体蛋白质组学分析系统性通路.
主要成果:
- 在rIR后的管状和免疫细胞中观察到增加的Gal-3表达.
- 当Gal-3存在于组织中时,功能障碍,损伤和炎症会加剧.
- 加尔-3上调与内皮激活和炎症相关,这些激活和炎症在Gal-3-/-小鼠中减少.
- 系统性Gal-3给药增加了中的CD146表达,但没有造成损伤.
- 隔离的管显示Gal-3与CD146相互作用,促进细胞因子分泌和免疫细胞透.
结论:
- 加列-3通过AKI的CD146相互作用促进内皮激活,导致损伤.
- 向Gal-3可能为AKI和相关的全身炎症提供治疗策略.
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