单细胞衍生的外体XIST通过调节miR-448-5p/HMGB2轴来加剧急性肺损伤
Shuyao Zhang1, Meini Chen2, Xinmin Guo3
1Department of Pharmacy, Guangzhou Red Cross Hospital, Jinan University, Guangzhou 510220, PR China; Department of Pharmacology, Shantou University Medical College, Shantou 515041, PR China.
International immunopharmacology
|July 4, 2023
概括
携带长非编码RNAXIST的单细胞衍生外体会通过抑制miR-448-5p和增加HMGB2.2来恶化急性肺损伤 (ALI). 这突出了ALI的新治疗标.
科学领域:
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
- 免疫学 免疫学 免疫学
背景情况:
- 单细胞衍生外体 (Exos) 在炎症性疾病中调解细胞间通信.
- 长非编码RNAs (lncRNAs) 在疾病发病过程中起着关键作用.
- 急性肺损伤 (ALI) 是一种严重的炎症状况,治疗选择有限.
研究的目的:
- 调查单细胞衍生异体性 lncRNA XIST 在 ALI 的启动和发展中的作用.
- 阐明外体XIST影响ALI进展的分子机制.
主要方法:
- 生物信息学预测ALI中的关键因素和监管机制.
- 建立一个脂聚糖 (LPS) 诱导的ALI小鼠模型.
- 在体外研究中,使用与已改造的Exos一起共同培养的HBE1细胞.
- 分子测定包括露西法酶记者,RIP和RNA拉下测定,以确认分子相互作用.
主要成果:
- 在LPS诱导的ALI中,XIST和HMGB2的调节上升,而miR-448-5p的调节下降.
- 单细胞衍生的Exos将XIST转移到HBE1细胞中,抑制miR-448-5p,并上调HMGB2.
- 在体内通过对miR-448-5p进行下调和对HMGB2.2进行上调来加剧外体XIST恶化的ALI.
结论:
- 单细胞衍生的外体XIST通过调节miR-448-5p/HMGB2信号轴来加剧ALI.
- 针对外体XIST/miR-448-5p/HMGB2通路可能为ALI提供治疗策略.
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