Tempol Preserves Endothelial Progenitor Cells in Male Mice with Ambient Fine Particulate Matter Exposure.

Xuanyou Liu,Hong Hao,Timothy L Domeier,Qinghua Sun,Zhiheng Chen,Zhenguo Liu,Yuqi Cui,Aimin Wang

doi:10.3390/biomedicines10020327

Xuanyou Liu, Hong Hao + Show 6 more

Open Access

https://doi.org/10.3390/biomedicines10020327

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Journal: Biomedicines	Publication Date: Jan 29, 2022
Citations: 5	License type: CC BY 4.0

Affiliation: University of Missouri, The Ohio State University

Abstract

Ambient fine particulate matter (PM) exposure associates with an increased risk of cardiovascular diseases (CVDs). Major sex differences between males and females exist in epidemiology, pathophysiology, and outcome of CVDs. Endothelial progenitor cells (EPCs) play a vital role in the development and progression of CVDs. PM exposure-induced reduction of EPCs is observed in male, not female, mice with increased reactive oxygen species (ROS) production and oxidative stress. The lung is considered an important source of ROS in mice with PM exposure. The aim of the present study was to investigate the sex differences in pulmonary superoxide dismutase (SOD) expression and ROS production, and to test the effect of SOD mimic Tempol on the populations of EPCs in mice with PM exposure. Both male and female C57BL/6 mice (8–10 weeks) were exposed to intranasal PM or vehicle for 6 weeks. Flow cytometry analysis demonstrated that PM exposure significantly decreased the levels of EPCs (CD34+/CD133+) in both blood and bone marrow with increased ROS production in males, but not in females. ELISA analysis showed higher levels of serum IL-6 and IL-1βin males than in females. Pulmonary expression of the antioxidant enzyme SOD1 was significantly decreased in males after PM exposure, but not in females. Administration of the SOD mimic Tempol in male mice with PM exposure attenuated the production of ROS and inflammatory cytokines, and preserved EPC levels. These data indicated that PM exposure-induced reduction of EPC population in male mice may be due to decreased expression of pulmonary SOD1 in male mice.

Highlights

Introduction published maps and institutional affilAmbient fine particulate matter (PM) is the key component of air pollution
Flow cytometry analysis was used to determine the levels of Endothelial progenitor cells (EPCs) in blood and bone marrow in mice following 6 weeks of PM exposure
No significant changes in EPC populations were observed in female mice with PM exposure (Figure 1A–C)

Summary

Introduction

Introduction published maps and institutional affilAmbient fine particulate matter (PM) is the key component of air pollution. Exposure to PM2.5 and PM0.1 are linked with increased cardiovascular morbidity and mortality as they can penetrate small airways and alveoli [2]. Long- or short-term PM2.5 exposure enhances the development and progression of cardiovascular diseases (CVDs), including ischemic heart disease, heart failure, arrhythmias, hypertension, and atherosclerosis [3,4]. Endothelial cell (EC) dysfunction plays a critical role in the pathogenesis of CVDs [5,6]. Endothelial progenitor cells (EPCs) that are primarily derived from bone marrow or tissueresident cells can restore dysfunctional endothelium and maintain normal cardiovascular function [7]. Abnormalities in the number and function of EPCs are closely related to CVDs including atherosclerosis and myocardial infarction [8,9].

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