An Atherogenic Diet Disturbs <i>Aquaporin 5</i> Expression in Liver and Adipocyte Tissues of Apolipoprotein E-Deficient Mice: New Insights into an Old Model of Experimental Atherosclerosis

• Published in: Biomedicines
• Main Authors: Inês V. da Silva, Courtney A. Whalen, Floyd J. Mattie, Cristina Florindo, Neil K. Huang, Sandra G. Heil, Thomas Neuberger, A. Catharine Ross, Graça Soveral, Rita Castro
• Format: Article
• Language: English
• Published: MDPI AG 2021-02-01
• Subjects: MRI (magnetic resonance imaging); endothelial dysfunction; high-fat diets; plaque burden
• Online Access: https://www.mdpi.com/2227-9059/9/2/150

The dysfunction of vascular endothelial cells is profoundly implicated in the pathogenesis of atherosclerosis and cardiovascular disease, the global leading cause of death. Aquaporins (AQPs) are membrane channels that facilitate water and glycerol transport across cellular membranes recently implicated in the homeostasis of the cardiovascular system. Apolipoprotein-E deficient (<i>apoE</i>^−/−) mice are a common model to study the progression of atherosclerosis. Nevertheless, the pattern of expression of <i>AQPs</i> in this atheroprone model is poorly characterized. In this study, <i>apoE</i>^−/− mice were fed an atherogenic high-fat (HF) or a control diet. Plasma was collected at multiple time points to assess metabolic disturbances. At the endpoint, the aortic atherosclerotic burden was quantified using high field magnetic resonance imaging. Moreover, the transcriptional levels of several <i>AQP</i> isoforms were evaluated in the liver, white adipocyte tissue (WAT), and brown adipocyte tissue (BAT). The results revealed that HF-fed mice, when compared to controls, presented an exacerbated systemic inflammation and atherosclerotic phenotype, with no major differences in systemic methylation status, circulating amino acids, or plasma total glutathione. Moreover, an overexpression of the isoform <i>AQP5</i> was detected in all studied tissues from HF-fed mice when compared to controls. These results suggest a novel role for AQP5 on diet-induced atherosclerosis that warrants further investigation.