Ex vivo coronary endothelial cell activation associated with indoor coal combustion initiated atherosclerosis

Plenty of rural populations still chronically exposed to indoor coal burning, which tremendously raises the risk of cardiovascular disease, in China. This study aimed to further investigate the association between indoor coal burning exposure and atherosclerotic cardiovascular diseases to search for...

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Veröffentlicht in:The Science of the total environment 2023-02, Vol.858 (Pt 3), p.160174, Article 160174
Hauptverfasser: Zhang, Wanjun, Pang, Yaxian, Cheng, Wenting, Wang, Tao, Li, Yanting, Li, Xin, Zhang, Jianzhong, Xia, Xiaowen, Zheng, Yuxin, Zhang, Rong, Tang, Jinglong
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container_end_page
container_issue Pt 3
container_start_page 160174
container_title The Science of the total environment
container_volume 858
creator Zhang, Wanjun
Pang, Yaxian
Cheng, Wenting
Wang, Tao
Li, Yanting
Li, Xin
Zhang, Jianzhong
Xia, Xiaowen
Zheng, Yuxin
Zhang, Rong
Tang, Jinglong
description Plenty of rural populations still chronically exposed to indoor coal burning, which tremendously raises the risk of cardiovascular disease, in China. This study aimed to further investigate the association between indoor coal burning exposure and atherosclerotic cardiovascular diseases to search for relevant markers for disease prevention. Herein, we conducted a cross-sectional study, carried out on 752 local long-term residents with or without bituminous coal for cooking and heating indoor, in Nangong County, Hebei Province, China. We utilized a nearest neighbor propensity score match (PSM) with a caliper distance equal to 0.001 to eliminate bias caused by confounding factors. The expression of genes associated with endothelial activation (CCL2, CCL5, CXCL8, CXCL12, VCAM, ICAM, SELP) in primary human coronary artery endothelial cells (HCAECs) were quantified through ex vivo biosensor assay. Multiple linear regression models with stratification analyses by gender and binary logit regression models were used to evaluate the association between mRNA expression of biosensor genes and indoor coal burning pollution or carotid atherosclerosis, respectively. Protein secretion level was detected by enzyme-linked immunosorbent assay (ELISA). The prevalence of carotid atherosclerosis in exposure group was higher than control (P = 0.023), before PSM. The gene expression of CCL2 in exposure group was significantly higher than control (P = 0.002). Indoor coal burning exposure was correlated with gene expression of CCL2 (β = 3.45, 95 % CI: 0.04–6.87, P = 0.047) and CXCL8 (β = 1.25, 95 % CI: 0.02–2.49, P = 0.046) in female. A higher risk of carotid atherosclerosis was observed in the same as the increase expression of CCL2 (OR = 1.07, 95 % CI: 1.01–1.14, P = 0.020). In conclusion, prolonged exposure to indoor coal burning could elevate the gene expression of CCL2 by activating vascular endothelial cells and was relative to the initiation of carotid atherosclerosis. [Display omitted] •Using an ex vivo biosensor assay based on propensity score matching to explore indoor coal burning mediated atherosclerosis.•Detected exact expression level of adhesion molecule and chemokines in biosensor cells by TaqMan qPCR assay.•Indoor coal burning exposure is more correlated with endothelial cell activation in female subjects.•Exposure population with higher CC-motif chemokine ligand 2 level have a higher atherosclerosis risk.
doi_str_mv 10.1016/j.scitotenv.2022.160174
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This study aimed to further investigate the association between indoor coal burning exposure and atherosclerotic cardiovascular diseases to search for relevant markers for disease prevention. Herein, we conducted a cross-sectional study, carried out on 752 local long-term residents with or without bituminous coal for cooking and heating indoor, in Nangong County, Hebei Province, China. We utilized a nearest neighbor propensity score match (PSM) with a caliper distance equal to 0.001 to eliminate bias caused by confounding factors. The expression of genes associated with endothelial activation (CCL2, CCL5, CXCL8, CXCL12, VCAM, ICAM, SELP) in primary human coronary artery endothelial cells (HCAECs) were quantified through ex vivo biosensor assay. Multiple linear regression models with stratification analyses by gender and binary logit regression models were used to evaluate the association between mRNA expression of biosensor genes and indoor coal burning pollution or carotid atherosclerosis, respectively. Protein secretion level was detected by enzyme-linked immunosorbent assay (ELISA). The prevalence of carotid atherosclerosis in exposure group was higher than control (P = 0.023), before PSM. The gene expression of CCL2 in exposure group was significantly higher than control (P = 0.002). Indoor coal burning exposure was correlated with gene expression of CCL2 (β = 3.45, 95 % CI: 0.04–6.87, P = 0.047) and CXCL8 (β = 1.25, 95 % CI: 0.02–2.49, P = 0.046) in female. A higher risk of carotid atherosclerosis was observed in the same as the increase expression of CCL2 (OR = 1.07, 95 % CI: 1.01–1.14, P = 0.020). In conclusion, prolonged exposure to indoor coal burning could elevate the gene expression of CCL2 by activating vascular endothelial cells and was relative to the initiation of carotid atherosclerosis. [Display omitted] •Using an ex vivo biosensor assay based on propensity score matching to explore indoor coal burning mediated atherosclerosis.•Detected exact expression level of adhesion molecule and chemokines in biosensor cells by TaqMan qPCR assay.•Indoor coal burning exposure is more correlated with endothelial cell activation in female subjects.•Exposure population with higher CC-motif chemokine ligand 2 level have a higher atherosclerosis risk.</description><identifier>ISSN: 0048-9697</identifier><identifier>EISSN: 1879-1026</identifier><identifier>DOI: 10.1016/j.scitotenv.2022.160174</identifier><identifier>PMID: 36379326</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>atherosclerosis ; Biosensor ; biosensors ; Carotid atherosclerosis ; China ; coal ; combustion ; coronary vessels ; cross-sectional studies ; disease prevention ; Endothelial activation ; endothelial cells ; environment ; enzyme-linked immunosorbent assay ; females ; gene expression ; humans ; Indoor coal burning pollution ; pollution ; Propensity score match ; protein secretion ; regression analysis ; risk</subject><ispartof>The Science of the total environment, 2023-02, Vol.858 (Pt 3), p.160174, Article 160174</ispartof><rights>2022 Elsevier B.V.</rights><rights>Copyright © 2022 Elsevier B.V. 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This study aimed to further investigate the association between indoor coal burning exposure and atherosclerotic cardiovascular diseases to search for relevant markers for disease prevention. Herein, we conducted a cross-sectional study, carried out on 752 local long-term residents with or without bituminous coal for cooking and heating indoor, in Nangong County, Hebei Province, China. We utilized a nearest neighbor propensity score match (PSM) with a caliper distance equal to 0.001 to eliminate bias caused by confounding factors. The expression of genes associated with endothelial activation (CCL2, CCL5, CXCL8, CXCL12, VCAM, ICAM, SELP) in primary human coronary artery endothelial cells (HCAECs) were quantified through ex vivo biosensor assay. Multiple linear regression models with stratification analyses by gender and binary logit regression models were used to evaluate the association between mRNA expression of biosensor genes and indoor coal burning pollution or carotid atherosclerosis, respectively. Protein secretion level was detected by enzyme-linked immunosorbent assay (ELISA). The prevalence of carotid atherosclerosis in exposure group was higher than control (P = 0.023), before PSM. The gene expression of CCL2 in exposure group was significantly higher than control (P = 0.002). Indoor coal burning exposure was correlated with gene expression of CCL2 (β = 3.45, 95 % CI: 0.04–6.87, P = 0.047) and CXCL8 (β = 1.25, 95 % CI: 0.02–2.49, P = 0.046) in female. A higher risk of carotid atherosclerosis was observed in the same as the increase expression of CCL2 (OR = 1.07, 95 % CI: 1.01–1.14, P = 0.020). In conclusion, prolonged exposure to indoor coal burning could elevate the gene expression of CCL2 by activating vascular endothelial cells and was relative to the initiation of carotid atherosclerosis. 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This study aimed to further investigate the association between indoor coal burning exposure and atherosclerotic cardiovascular diseases to search for relevant markers for disease prevention. Herein, we conducted a cross-sectional study, carried out on 752 local long-term residents with or without bituminous coal for cooking and heating indoor, in Nangong County, Hebei Province, China. We utilized a nearest neighbor propensity score match (PSM) with a caliper distance equal to 0.001 to eliminate bias caused by confounding factors. The expression of genes associated with endothelial activation (CCL2, CCL5, CXCL8, CXCL12, VCAM, ICAM, SELP) in primary human coronary artery endothelial cells (HCAECs) were quantified through ex vivo biosensor assay. Multiple linear regression models with stratification analyses by gender and binary logit regression models were used to evaluate the association between mRNA expression of biosensor genes and indoor coal burning pollution or carotid atherosclerosis, respectively. Protein secretion level was detected by enzyme-linked immunosorbent assay (ELISA). The prevalence of carotid atherosclerosis in exposure group was higher than control (P = 0.023), before PSM. The gene expression of CCL2 in exposure group was significantly higher than control (P = 0.002). Indoor coal burning exposure was correlated with gene expression of CCL2 (β = 3.45, 95 % CI: 0.04–6.87, P = 0.047) and CXCL8 (β = 1.25, 95 % CI: 0.02–2.49, P = 0.046) in female. A higher risk of carotid atherosclerosis was observed in the same as the increase expression of CCL2 (OR = 1.07, 95 % CI: 1.01–1.14, P = 0.020). In conclusion, prolonged exposure to indoor coal burning could elevate the gene expression of CCL2 by activating vascular endothelial cells and was relative to the initiation of carotid atherosclerosis. [Display omitted] •Using an ex vivo biosensor assay based on propensity score matching to explore indoor coal burning mediated atherosclerosis.•Detected exact expression level of adhesion molecule and chemokines in biosensor cells by TaqMan qPCR assay.•Indoor coal burning exposure is more correlated with endothelial cell activation in female subjects.•Exposure population with higher CC-motif chemokine ligand 2 level have a higher atherosclerosis risk.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>36379326</pmid><doi>10.1016/j.scitotenv.2022.160174</doi></addata></record>
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source Elsevier ScienceDirect Journals
subjects atherosclerosis
Biosensor
biosensors
Carotid atherosclerosis
China
coal
combustion
coronary vessels
cross-sectional studies
disease prevention
Endothelial activation
endothelial cells
environment
enzyme-linked immunosorbent assay
females
gene expression
humans
Indoor coal burning pollution
pollution
Propensity score match
protein secretion
regression analysis
risk
title Ex vivo coronary endothelial cell activation associated with indoor coal combustion initiated atherosclerosis
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