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Author Spotlight: Modeling an Aspect of Preeclampsia in Female Mice Using Hypoxic Human Placenta-Derived Small Extracellular Vesicles

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Red blood cells from patients with pre-eclampsia induce endothelial dysfunction.

Sarah M McCann Haworth¹, Zhengbing Zhuge¹, Carina Nihlén¹

¹Department of Physiology and Pharmacology.

Journal of Hypertension

|March 3, 2021

Summary

Red blood cells (RBCs) in pre-eclampsia increase arginase activity, causing endothelial dysfunction via nitric oxide (NO) reduction and oxidative stress. Targeting RBC arginase may offer a new treatment for pre-eclampsia.

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Published on: November 20, 2015

Area of Science:

Cardiovascular Research
Obstetrics and Gynecology
Vascular Biology

Background:

Pre-eclampsia is a pregnancy disorder characterized by systemic vascular dysfunction and reduced nitric oxide (NO) bioavailability.
Arginase competes with NO synthase (NOS) for L-arginine, potentially decreasing NO production and increasing reactive oxygen species (ROS), leading to endothelial dysfunction.
Red blood cells (RBCs) play a crucial role in NO homeostasis, and their abnormal arginase function is linked to oxidative stress and endothelial dysfunction in conditions like diabetes.

Purpose of the Study:

To investigate whether reduced NO bioavailability and increased ROS in pre-eclampsia are mediated by RBC-dependent mechanisms.
To explore the role of RBC arginase activity and expression in the pathogenesis of pre-eclampsia-associated endothelial dysfunction.

Main Methods:

Plasma and RBCs were isolated from women with pre-eclampsia and healthy pregnant women.
Mouse aortas were co-incubated with isolated plasma and RBCs to assess vascular reactivity.
NO bioactivity markers (nitrate, nitrite, cGMP), arginase activity and expression in RBCs, and markers of oxidative stress were analyzed.

Main Results:

Plasma NO markers were decreased in pre-eclamptic women.
Co-incubation with pre-eclamptic RBCs, but not healthy RBCs, induced endothelial dysfunction in mouse aortas.
This dysfunction was ameliorated by inhibiting arginase, scavenging ROS, or nitrite treatment, and was linked to increased RBC arginase activity and expression, correlating with pre-eclampsia severity.

Conclusions:

Red blood cells play a significant role in mediating endothelial dysfunction in pre-eclampsia through arginase-dependent mechanisms and oxidative stress.
Elevated RBC arginase activity contributes to reduced NO bioavailability and increased ROS in pre-eclampsia.
Targeting RBC arginase presents a potential novel therapeutic strategy for managing pre-eclampsia.