Abstract
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 (apoE−/−) mice are a common model to study the progression of atherosclerosis. Nevertheless, the pattern of expression of AQPs in this atheroprone model is poorly characterized. In this study, apoE−/− 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 AQP 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 AQP5 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.
Highlights
Despite significant advances in the treatment of cardiovascular disease (CVD), it remains the leading cause of mortality and morbidity among adults [1]
Our previous work revealed that AQP7 and AQP9 are downregulated along the browning process, which may be related to the physiological role of brown adipocyte tissue (BAT) in heat production, contrasting with the anabolic/catabolic lipid metabolism in white adipose cells [26]
To investigate whether a HF diet would disturb the expression of AQPs in an atherosclerosis prone model, we fed apoE−/− mice HF or control diets
Summary
Despite significant advances in the treatment of cardiovascular disease (CVD), it remains the leading cause of mortality and morbidity among adults [1]. Our previous work revealed that AQP7 and AQP9 are downregulated along the browning process, which may be related to the physiological role of BAT in heat production, contrasting with the anabolic/catabolic lipid metabolism in white adipose cells [26]. The functional importance of AQP1 to maintain endothelial homeostasis and cardiovascular health in humans and mice has been recently reported [4]. We postulated that an atherogenic diet would disturb AQPs expression profile, allowing the identification of the AQPs isoforms related with vascular toxicity To investigate this possibility male apoE−/− mice were fed high-fat (HF) or control diets. After confirming a strong atherosclerotic phenotype in the HF-fed mice, we determined the mRNA expressions of the orthodox isoforms, AQP1 and AQP5, and of the aquaglyceroporins AQP3, AQP7, and AQP9, in different metabolic tissues (BAT, WAT, and liver)
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