학술논문

IL-17A promotes vascular calcification in an ex vivo murine aorta culture.
Document Type
Article
Source
Biochemical & Biophysical Research Communications. May2022, Vol. 604, p83-87. 5p.
Subject
*ARTERIAL calcification
*AORTA
*ABDOMINAL aorta
*X-ray computed microtomography
*SKIN diseases
*CARDIOVASCULAR diseases risk factors
Language
ISSN
0006-291X
Abstract
Vascular calcification is characterized by mineral deposition in the vasculature, which is triggered by chronic systemic inflammation, including psoriasis. Psoriasis is an IL-17A-mediated inflammatory skin disease that is associated with exacerbated vascular calcification and high cardiovascular mortality. Although previous studies have shown that IL-17A induces vascular dysfunction in murine psoriasis models, it has not been clarified whether IL-17A induces vascular calcification. In this study, we investigated the potential vascular calcification-inducing effect of IL-17A in an ex vivo culture system. Thoracic and abdominal aortas from mice were cultured in a medium supplemented with inorganic phosphate and were treated with inflammatory cytokines (IL-1β, TNF-α, IL-6, and IL-17A). Vascular calcification was determined using micro-computed tomography (CT) and histological analyses. IL-1β, TNF-α, and IL-6 did not significantly promote vascular calcification, whereas IL-17A significantly accelerated vascular calcification of the aorta, as indicated by the increased mineralized volume based on micro-CT analysis. Micro-CT and histological analyses also revealed that the promoting effect of IL-17A on vascular calcification was concentration dependent. IL-17A significantly promoted vascular calcification in ex vivo cultured aortas, which suggests that this mechanism is involved in the increased risk of cardiovascular events in IL-17A-mediated inflammatory diseases. • IL-17A-mediated inflammatory diseases, including psoriasis, are associated with increased cardiovascular events. • IL-17A promotes vascular calcification in an ex vivo murine aorta culture. [ABSTRACT FROM AUTHOR]