Urban fine particulate air pollution exposure promotes atherosclerosis in apolipoprotein E-deficient mice by activating perivascular adipose tissue inflammation via the Wnt5a/Ror2 signaling pathway

Urban fine particulate matter (PM2.5) is a deleterious risk factor in the ambient air and is recognized to exacerbate atherosclerosis. Perivascular adipose tissue (PVAT) secretes a large number of inflammatory cytokines and plays a crucial role in the pathogenic microenvironment of atherogenesis. Ho...

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Autores principales:	Qiang Wan, Tao Ding, Yulin Xu, Cuicui Zheng, Mengting Tu, Tong Zhao
Formato:	article
Lenguaje:	EN
Publicado:	Elsevier 2021
Materias:	Fine particulate matter Perivascular adipose tissue Inflammation Atherosclerosis Wnt5a/Ror2 pathway Environmental pollution TD172-193.5 Environmental sciences GE1-350
Acceso en línea:	https://doaj.org/article/8b5c22c06ac141b4b747f0aeb5c85560
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spelling	oai:doaj.org-article:8b5c22c06ac141b4b747f0aeb5c855602021-11-06T04:16:56ZUrban fine particulate air pollution exposure promotes atherosclerosis in apolipoprotein E-deficient mice by activating perivascular adipose tissue inflammation via the Wnt5a/Ror2 signaling pathway0147-651310.1016/j.ecoenv.2021.112912https://doaj.org/article/8b5c22c06ac141b4b747f0aeb5c855602021-12-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S0147651321010241https://doaj.org/toc/0147-6513Urban fine particulate matter (PM2.5) is a deleterious risk factor in the ambient air and is recognized to exacerbate atherosclerosis. Perivascular adipose tissue (PVAT) secretes a large number of inflammatory cytokines and plays a crucial role in the pathogenic microenvironment of atherogenesis. However, there is a lack of knowledge about the role of PVAT inflammation in the genesis of PM2.5-related atherosclerosis. The aim of this research was to probe the latent links between PM2.5 exposure and PVAT inflammation and further discovered the underlying mechanisms of PM2.5-triggered atherosclerosis pathogenesis. Apolipoprotein E-deficient (ApoE−/−) mice were exposed to real-world atmospheric PM2.5 or filtered clean air for three months, the Wnt5a inhibitor Box5 and the Ror2 inhibitor β-Arrestin2 were applied to verify the possible mechanisms. We noticed that the average daily PM2.5 mass concentration was 84.27 ± 28.84 μg/m3. PM2.5 inhalation might significantly expedite the deterioration of atherosclerosis, increase the protein and mRNA expressions of MCP-1, IL-6, TNF-α, Wnt5a, and Ror2 in PVAT tissues, upregulate the distributions of IL-6, TNF-α, MCP-1, and leptin in the histological sections of PVAT, promote lipid deposition in the aorta, elevate the plasma levels of leptin, MCP-1, IL-6, TNF-α, LDL-C, TC, and TG, however, decrease the plasma levels of adiponectin and HDL-C, downregulate the distribution of adiponectin. Nevertheless, these effects caused by PM2.5 exposure were dramatically diminished after the administration of Box5 or β-Arrestin2. This research illuminated that PVAT inflammation was involved in the PM2.5-induced atherosclerosis process, as well as lipid deposition, which was closely associated with the activation of the Wnt5a/Ror2 signaling pathway.Qiang WanTao DingYulin XuCuicui ZhengMengting TuTong ZhaoElsevierarticleFine particulate matterPerivascular adipose tissueInflammationAtherosclerosisWnt5a/Ror2 pathwayEnvironmental pollutionTD172-193.5Environmental sciencesGE1-350ENEcotoxicology and Environmental Safety, Vol 227, Iss , Pp 112912- (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Fine particulate matter Perivascular adipose tissue Inflammation Atherosclerosis Wnt5a/Ror2 pathway Environmental pollution TD172-193.5 Environmental sciences GE1-350
spellingShingle	Fine particulate matter Perivascular adipose tissue Inflammation Atherosclerosis Wnt5a/Ror2 pathway Environmental pollution TD172-193.5 Environmental sciences GE1-350 Qiang Wan Tao Ding Yulin Xu Cuicui Zheng Mengting Tu Tong Zhao Urban fine particulate air pollution exposure promotes atherosclerosis in apolipoprotein E-deficient mice by activating perivascular adipose tissue inflammation via the Wnt5a/Ror2 signaling pathway
description	Urban fine particulate matter (PM2.5) is a deleterious risk factor in the ambient air and is recognized to exacerbate atherosclerosis. Perivascular adipose tissue (PVAT) secretes a large number of inflammatory cytokines and plays a crucial role in the pathogenic microenvironment of atherogenesis. However, there is a lack of knowledge about the role of PVAT inflammation in the genesis of PM2.5-related atherosclerosis. The aim of this research was to probe the latent links between PM2.5 exposure and PVAT inflammation and further discovered the underlying mechanisms of PM2.5-triggered atherosclerosis pathogenesis. Apolipoprotein E-deficient (ApoE−/−) mice were exposed to real-world atmospheric PM2.5 or filtered clean air for three months, the Wnt5a inhibitor Box5 and the Ror2 inhibitor β-Arrestin2 were applied to verify the possible mechanisms. We noticed that the average daily PM2.5 mass concentration was 84.27 ± 28.84 μg/m3. PM2.5 inhalation might significantly expedite the deterioration of atherosclerosis, increase the protein and mRNA expressions of MCP-1, IL-6, TNF-α, Wnt5a, and Ror2 in PVAT tissues, upregulate the distributions of IL-6, TNF-α, MCP-1, and leptin in the histological sections of PVAT, promote lipid deposition in the aorta, elevate the plasma levels of leptin, MCP-1, IL-6, TNF-α, LDL-C, TC, and TG, however, decrease the plasma levels of adiponectin and HDL-C, downregulate the distribution of adiponectin. Nevertheless, these effects caused by PM2.5 exposure were dramatically diminished after the administration of Box5 or β-Arrestin2. This research illuminated that PVAT inflammation was involved in the PM2.5-induced atherosclerosis process, as well as lipid deposition, which was closely associated with the activation of the Wnt5a/Ror2 signaling pathway.
format	article
author	Qiang Wan Tao Ding Yulin Xu Cuicui Zheng Mengting Tu Tong Zhao
author_facet	Qiang Wan Tao Ding Yulin Xu Cuicui Zheng Mengting Tu Tong Zhao
author_sort	Qiang Wan
title	Urban fine particulate air pollution exposure promotes atherosclerosis in apolipoprotein E-deficient mice by activating perivascular adipose tissue inflammation via the Wnt5a/Ror2 signaling pathway
title_short	Urban fine particulate air pollution exposure promotes atherosclerosis in apolipoprotein E-deficient mice by activating perivascular adipose tissue inflammation via the Wnt5a/Ror2 signaling pathway
title_full	Urban fine particulate air pollution exposure promotes atherosclerosis in apolipoprotein E-deficient mice by activating perivascular adipose tissue inflammation via the Wnt5a/Ror2 signaling pathway
title_fullStr	Urban fine particulate air pollution exposure promotes atherosclerosis in apolipoprotein E-deficient mice by activating perivascular adipose tissue inflammation via the Wnt5a/Ror2 signaling pathway
title_full_unstemmed	Urban fine particulate air pollution exposure promotes atherosclerosis in apolipoprotein E-deficient mice by activating perivascular adipose tissue inflammation via the Wnt5a/Ror2 signaling pathway
title_sort	urban fine particulate air pollution exposure promotes atherosclerosis in apolipoprotein e-deficient mice by activating perivascular adipose tissue inflammation via the wnt5a/ror2 signaling pathway
publisher	Elsevier
publishDate	2021
url	https://doaj.org/article/8b5c22c06ac141b4b747f0aeb5c85560
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Urban fine particulate air pollution exposure promotes atherosclerosis in apolipoprotein E-deficient mice by activating perivascular adipose tissue inflammation via the Wnt5a/Ror2 signaling pathway

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