ECE2022 Eposter Presentations General Endocrinology (15 abstracts)
Exposure to the endocrine disruptor cadmium alters human aortic endothelial cells homeostasis
Giuseppina Catanzaro 1 , Claudia Sabato 1 , Viviana Maria Bimonte 2 , Zaira Spinello 1 , Agnese Po 3 , Zein Mersini Besharat 1 , Alessandra Vacca 1 , Silvia Migliaccio 2 & Elisabetta Ferretti 1
1Sapienza University, Experimental Medicine, Rome, Italy; 2Foro Italico University, Movement, Human & Health Sciences, Rome, Italy; 3Sapienza University, Molecular Medicine, Rome, Italy
Cardiovascular diseases (CVDs) represent a complex and multifactorial issue that results from a combination of behavioural, genetic and environmental factors. Toxic metal contaminants, many of which act as endocrine disruptors (EDs), have been identified as potential risk factors for CVDs. Among EDs Cadmium (Cd), present both in cigarettes and in food, has been suggested to be cytotoxic on vascular endothelium, likely leading to blood pressure increase and vascular inflammation. We previously demonstrated that Cd exposure increased TNF-α, IL-6 and IL-8 mRNA in HUVEC endothelial cells. The aim of this study was to further evaluate and characterize the potentially detrimental effect of Cd exposure on Endothelial cells. The effect of Cd exposure on the vascular system was evaluated by using a human in-vitro model for vascular endothelial cells, the human Aortic Endothelial Cells (HAEC). Firstly, we evaluated HAEC morphology after 24 h exposure to increasing Cd concentrations, ranging from 1 to 10 μM. Cd induced a collapse of cytoskeleton, with a toxic effect already evident upon treatment with 1 μM. The effect on cellular morphology was accompanied by a reduction of cell proliferation and an increase in cell death. In addition, the Bax/Bcl2 ratio increased. Moreover, Cd affected the expression of pro-inflammatory cytokines, showing an increase of both IL-6 and IL-8 upon 5 and 10 μM Cd exposure, confirming our previous results obtained in HUVEC. Accordingly, a decrease of endothelial adhesion molecules, such as V-CAM and I-CAM, was observed. In conclusion, our results suggest that Cd exposure affects HAEC morphology and behaviour inducing cytotoxicity and apoptosis. In addition, already at low concentration, Cd exposure induces a pro-inflammatory state with production of pro-inflammatory cytokines and reduction of endothelial adhesion molecules, strongly suggesting that this heavy metal is able to alter endothelium homeostasis.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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