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Quantification of Atherosclerosis in Mice

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Published on: June 12, 2019

Chronic Inhaled Benzene Exposure Exacerbates Atherosclerosis in LDL Receptor-Null Mice.

Igor N Zelko^1,2,3, Marina V Malovichko^1,2,3, Samantha A McFall^1,2,3,4

¹University of Louisville Superfund Research Center.

Biorxiv : the Preprint Server for Biology

|February 20, 2025

Summary

Inhaled benzene accelerates atherosclerosis by increasing vascular inflammation and T-cell proliferation in LDL receptor knockout mice. This exposure also impacts smooth muscle cells, potentially reducing plaque stability and promoting platelet activation.

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Area of Science:

Environmental toxicology
Cardiovascular research
Immunology

Background:

Benzene is a widespread environmental pollutant and a known carcinogen.
Its potential role in atherosclerosis (hardening of the arteries) is not well understood.

Purpose of the Study:

To investigate the impact of inhaled benzene on the development of atherosclerosis.
To explore the underlying mechanisms involving vascular inflammation and immune cell responses.

Main Methods:

Exposure of male LDL receptor knockout (LDLR-KO) mice to benzene or filtered air.
Dietary intervention with a western diet during the exposure period.
Analysis of aortic tissue using single-nuclei RNA sequencing (snRNAseq).
In vitro experiments with T cells and hydroquinone (HQ) to assess ROR-gamma levels.

Main Results:

Benzene inhalation significantly increased aortic valve lesion area in LDLR-KO mice.
Increased numbers of T cells and proliferating T cells were observed in benzene-exposed aortae.
Benzene altered gene expression in T cells, promoting Th17 polarization and affecting apoptosis regulators.
Changes in vascular smooth muscle cells (VSMC) included downregulation of extracellular matrix genes and upregulation of platelet degranulation pathways.

Conclusions:

Inhaled benzene exposure exacerbates atherosclerosis by promoting T-cell proliferation and Th17 polarization.
Benzene exposure negatively affects plaque stability through VSMC alterations and platelet activation.
These findings highlight benzene as a risk factor for cardiovascular disease.