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Secreted Monocyte miR-27a, via Mesenteric Arterial Mas Receptor-eNOS Pathway, Causes Hypertension
Xue Zou1,2, Jialiang Wang1,2, Caiyu Chen1,2
1Department of Cardiology, Daping Hospital, The Third Military Medical University, Chongqing, P.R. China.
Background:
Essential hypertension is associated with increased plasma concentrations of extracellular vesicles (EVs). We aimed to determine the role of monocyte miR-27a in EVs on arterial Mas receptor expression, and its involvement in the pathogenesis of hypertension.
Methods:
THP-1 cells were transfected with miR-27a mimic and miR-27a inhibitor, and EVs were collected. Mas receptor expression and endothelial nitric oxide synthase (eNOS) phosphorylation were determined by immunoblotting. Sprague-Dawley (SD) rats received EVs via tail-vein injection. Blood pressure (BP) was measured with the tail-cuff method. The vasodilatory response of mesenteric arteries was measured using a small vessel myograph.
Results:
EVs from THP-1 cells increased rat BP by impairing Ang-(1-7)-mediated vasodilation in mesenteric arteries, which was further exaggerated by EVs from lipopolysaccharides-treated THP-1 cells. As the receptor and key signaling of Ang-(1-7), next experiments found that Mas receptor expression and eNOS phosphorylation were decreased in mesenteric arteries from EVs-treated SD rats. Screening studies found miR-27a in EVs may be involved in this process. Through transfection with miR-27a inhibitor or miR-27a mimic, we found that miR-27a downregulates Mas receptor expression in endothelial cells. Injection of EVs from miR-27a-transfected HEK-293 cells decreased Mas receptor and eNOS phosphorylation in mesenteric arteries, impaired Ang-(1-7)-mediated vasodilation and increased BP. Earlier effects were reversed using cells with downregulation of miR-27 in EVs.
Conclusions:
Monocyte miR-27a in EVs decreases Mas receptor expression and eNOS phosphorylation in endothelium, impairs Ang-(1-7)-mediated vasodilation, and causes hypertension. Understanding the contributions of EVs in the pathogenesis of hypertension may facilitate their use as a diagnostic biomarker.
Insights
Monocyte microRNA-27a (miR-27a) in extracellular vesicles (EVs) reduces Mas receptor expression, impairing vasodilation and increasing blood pressure. This highlights EVs
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Cell Biology
Background:
- Essential hypertension is linked to elevated extracellular vesicle (EV) concentrations in plasma.
- The specific role of monocyte-derived EVs, particularly microRNA-27a (miR-27a), in hypertension pathogenesis remains unclear.
Purpose of the Study:
- To investigate the function of monocyte miR-27a within EVs concerning arterial Mas receptor expression.
- To elucidate the involvement of monocyte miR-27a in EVs in the development of hypertension.
Main Methods:
- THP-1 cells were manipulated for miR-27a expression, and resultant EVs were analyzed.
- Mas receptor expression and eNOS phosphorylation were assessed via immunoblotting.
- EVs were administered to Sprague-Dawley rats to measure blood pressure and mesenteric artery vasodilation.
Main Results:
- EVs from miR-27a-manipulated cells decreased Mas receptor expression and eNOS phosphorylation in rat mesenteric arteries.
- EV administration elevated blood pressure and impaired Ang-(1-7)-mediated vasodilation.
- miR-27a within EVs was identified as a key mediator in downregulating Mas receptor expression and contributing to hypertension.
Conclusions:
- Monocyte miR-27a packaged in EVs contributes to hypertension by reducing Mas receptor expression and endothelial nitric oxide synthase (eNOS) phosphorylation.
- This mechanism impairs vasodilation and promotes elevated blood pressure.
- EVs may serve as potential diagnostic biomarkers for hypertension.
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