间歇性缺氧处理红细胞衍生的细胞外囊泡通过调节 eNOS 磷酸化和 ET-1 表达损害内皮功能

核心信息

• 论文英文标题: Extracellular Vesicles Derived from Intermittent Hypoxia–Treated Red Blood Cells Impair Endothelial Function Through Regulating eNOS Phosphorylation and ET-1 Expression
• 期刊: Cardiovasc Drug Ther
• 发表年份: 2020
• DOI: 10.1007/s10557-020-07117-3
• PMID/PMCID: 33242203; 27188535

研究概览

The aim of this research is to clarify whether and how EVs shedding from red blood cells (RBCs) are involved in IH-induced endothelial dysfunction. However, the underlying mechanism still remains unclear.

核心发现

Functional results demonstrated that REVs from OSA patients dramatically impaired endothelium-dependent relaxations (EDRs).

Similarly, in vivo and ex vivo studies showed that IH REVs caused significant endothelial dysfunction compared to control group.

Further results presented that IH REVs blocked endothelial nitric oxide synthase (eNOS) phosphorylation through inhibiting PI3K/Akt pathway and enhanced endothelin-1 (ET-1) expression through activating Erk1/2 pathway in endothelial cells.

Meanwhile, endothelial dysfunction caused by IH REVs was reversed by Akt activator SC79 as well as Erk kinase inhibitor PD98059, suggesting that PI3K/Akt/eNOS and Erk1/2/ET-1 pathways were implicated in IH REV-induced impaired EDRs.

研究设计

EVs were extracted by ultracentrifugation.

After the identification of property and purity, EVs from IH-exposed RBCs (IH REVs) and normoxia-exposed RBCs (NOR REVs) or from OSA and non-OSA patient RBCs were utilized to treat C57BL/6 mouse aortas or human umbilical vein endothelial cells (HUVECs) for mechanistic exploration.

Echo Biotech 角色

电镜鉴定

关联平台: Exoomics®

关联服务与能力: EV Basic Characterization (TEM/NTA/WB)

关联产品或试剂: 无明确产品引用

参考文献

原始论文: Extracellular Vesicles Derived from Intermittent Hypoxia–Treated Red Blood Cells Impair Endothelial Function Through Regulating eNOS Phosphorylation and ET-1 Expression Cardiovasc Drug Ther. 2020. DOI: 10.1007/s10557-020-07117-3. PMID/PMCID: 33242203; 27188535.