Extracellular vesicles (EVs) are novel mediators of cell-to-cell communication and appear to mediate the pathogenesis of hypertension (HTN). However, the mechanisms underlying the involvement of EVs in HTN remain unclear. The adaptive and innate immune systems (IS) play an important role affecting the kidney and vasculature in animal models of HTN. Evolving evidence shows that immune cell-derived EVs can modulate the IS in a paracrine fashion and therefore may mediate the effects of inflammation in the pathogenesis of HTN. Therefore, we aimed to understand if specific subtypes of leukocyte/immune-cell-derived EVs are altered in essential HTN using an in-vivo model of Angiotensin-II induced HTN. After 4 weeks of Ang II treatment, EVs were isolated from blood and kidney. EV's origin and counts were characterized with using flow cytometry, antibody panels targeting platelets, endothelial cells, and leukocytes including B- and T-cells, monocytes, and neutrophils. Leukocyte (CD45+) EVs were elevated in the circulation and kidney tissue in Ang-II HTN. Subgroup analysis depicted T-cell derived EVs (CD3+) to be significantly elevated in Ang-II induced HTN (3.50E+05 particles/ml) compared to control groups (9.16E+04 particles/ml, p=0.0106). T-cell derived EVs also significantly correlated with systolic blood pressure (BP) levels (r²= 0.898; p=0.0012). In summary, leukocyte-derived EVs and more specifically T-cell-derived EVs (CD3+) are elevated in Ang-II induced HTN in the circulation and kidney tissue and correlate well with BP severity. EVs from the circulation and kidney may be sensitive biomarkers for HTN and end-organ damage and may lead to new mechanistic insights in this silent disease.

中文翻译：

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T 细胞来源的细胞外囊泡在必需 HTN 中升高

细胞外囊泡（EV）是细胞间通讯的新型介质，似乎介导高血压（HTN）的发病机制。然而，EV 参与 HTN 的机制仍不清楚。在 HTN 动物模型中，适应性和先天免疫系统 (IS) 在影响肾脏和脉管系统方面发挥着重要作用。不断变化的证据表明，免疫细胞衍生的 EV 可以旁分泌方式调节 IS，因此可能介导炎症对 HTN 发病机制的影响。因此，我们的目的是使用血管紧张素-II 诱导的 HTN 体内模型来了解白细胞/免疫细胞来源的 EV 的特定亚型是否在基本 HTN 中发生改变。Ang II 治疗 4 周后，从血液和肾脏中分离出 EV。使用流式细胞术、针对血小板、内皮细胞和白细胞（包括 B 细胞和 T 细胞、单核细胞和中性粒细胞）的抗体组来表征 EV 的起源和计数。Ang-II HTN 中循环和肾组织中的白细胞 (CD45+) EV 升高。亚组分析显示，与对照组（9.16E+04 颗粒/ml，p=0.0106）相比，Ang-II 诱导的 HTN（3.50E+05 颗粒/ml）中 T 细胞衍生的 EV（CD3+）显着升高。T 细胞衍生的 EV 还与收缩压 (BP) 水平显着相关 (r ² = 0.898；p=0.0012)。总之，白细胞衍生的 EV，更具体地说，T 细胞衍生的 EV (CD3+) 在循环和肾组织中 Ang-II 诱导的 HTN 中升高，并且与血压严重程度密切相关。来自循环和肾脏的 EV 可能是 HTN 和终末器官损伤的敏感生物标志物，并可能为这种无声疾病带来新的机制见解。