Aims

Endothelial microparticles (EMPs) are extracellular vesicles secreted by endothelial cells. The purpose of this research is to explore that the clinical significance and roles in angiogenesis and endothelial dysfunction of circulating microparticles in Perthes disease.

Main methods

We collected platelet-poor plasma (PPP) from patients and controls, then microparticles (MPs) were extracted. Flow cytometry was performed to calculate the concentrations of CD31+/CD42b-, CD62E+ and CD31+/CD42b+ MPs. ELISA was performed to detect the expression level of biomarkers of endothelial dysfunction and inflammatory factors in plasma. In vitro experiments to evaluate the effect of circulating MPs and EMPs derived from IL-6-stimulated human umbilical vein endothelial cells (HUVECs) on angiogenesis and endothelial dysfunction.

Key findings

Our results revealed that the CD31+/CD42b- EMPs were significantly higher in Perthes disease group than in the control group. The Perthes-MPs being taken up by HUVECs promoted endothelial cell apoptosis, endothelial dysfunction and inhibited angiogenesis in vitro. Moreover, the level of IL-6 in plasma significantly increased in patients with Perthes, which was tightly correlated with the elevated level of circulating CD31+/CD42b- EMPs. IL-6 promoted HUVECs to secrete CD31+/CD42b- MPs, and EMPs derived from high concentration IL-6-stimulated (100 and 1000 pg/mL) HUVECs promoted endothelial cell apoptosis, endothelial dysfunction and inhibited angiogenesis.

Significance

In summary, our study suggests that circulating EMPs in the phenotypic spectrum revealed unique phenotypes of endothelial dysfunction, showing close correlation with the secretion of IL-6. These circulating EMPs may give rise to endothelial cell apoptosis, endothelial dysfunction and angiogenesis in Perthes disease.

中文翻译：

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Perthes病中循环CD31 + / CD42b-EMPs增加并通过内皮功能障碍抑制HUVEC血管生成

目的

内皮微粒（EMPs）是内皮细胞分泌的细胞外囊泡。本研究的目的是探讨Perthes病中循环微粒的血管生成和内皮功能障碍的临床意义和作用。

主要方法

我们从患者和对照中收集贫血小板血浆（PPP），然后提取微粒（MPs）。进行流式细胞术以计算CD31 + / CD42b-，CD62E +和CD31 + / CD42b + MP的浓度。进行ELISA以检测血浆中内皮功能障碍和炎症因子的生物标志物的表达水平。体外实验，评估源自IL-6刺激的人脐静脉内皮细胞（HUVEC）的循环MP和EMP对血管生成和内皮功能障碍的影响。

主要发现

我们的结果显示，Perthes疾病组的CD31 + / CD42b- EMPs明显高于对照组。HUVECs摄取的Perthes-MPs在体外促进内皮细胞凋亡，内皮功能障碍并抑制血管生成。此外，Perthes患者的血浆IL-6水平显着升高，这与循环CD31 + / CD42b-EMPs水平升高密切相关。IL-6促进HUVEC分泌CD31 + / CD42b- MP，而高浓度IL-6刺激（100和1000 pg / mL）的EMP促进内皮细胞凋亡，内皮功能障碍并抑制血管生成。

意义

总之，我们的研究表明，在表型谱中循环的EMPs揭示了内皮功能障碍的独特表型，与IL-6的分泌密切相关。这些循环的EMPs可能导致Perthes病中的内皮细胞凋亡，内皮功能障碍和血管生成。