The effects of cooking oil fumes-derived PM2.5 on blood vessel formation through ROS-mediated NLRP3 inflammasome pathway in human umbilical vein endothelial cells

Cooking oil fumes (COFs), a main pollutant in kitchen air, is a major risk to human health. In our previous research, exposure to COFs-derived PM2.5 could cause umbilical vascular endothelial dysfunction, leading to decreased fetal weight. Here, to test the role of ROS-mediated NLRP3 inflammasome pa...

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Veröffentlicht in:Ecotoxicology and environmental safety 2019-06, Vol.174, p.690-698
Hauptverfasser: Shen, Chaowei, Liu, Jie, Zhu, Furong, Lei, Ruoqian, Cheng, Han, Zhang, Chao, Sui, Xinmiao, Ding, Liu, Yang, Mei, Chen, Hongbo, Ding, Rui, Cao, Jiyu
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container_issue
container_start_page 690
container_title Ecotoxicology and environmental safety
container_volume 174
creator Shen, Chaowei
Liu, Jie
Zhu, Furong
Lei, Ruoqian
Cheng, Han
Zhang, Chao
Sui, Xinmiao
Ding, Liu
Yang, Mei
Chen, Hongbo
Ding, Rui
Cao, Jiyu
description Cooking oil fumes (COFs), a main pollutant in kitchen air, is a major risk to human health. In our previous research, exposure to COFs-derived PM2.5 could cause umbilical vascular endothelial dysfunction, leading to decreased fetal weight. Here, to test the role of ROS-mediated NLRP3 inflammasome pathway in blood vessel formation of human umbilical vein endothelial cells (HUVECs) caused by COFs-derived PM2.5, the cells were exposed to COFs-derived PM2.5 at different concentrations with and without N-acetyl-L-cysteine (NAC). MTT assay was used to determine HUVECs viability. Intracellular ROS and mitochondrial ROS levels were assessed with DCFH-DA and MitoSOX™ assay. The levels of proteins and mRNA involved in NLRP3 inflammasome signaling pathway and VEGF were measured by western blot and real-time PCR (RT-PCR). Tube formation in HUVECs was detected by tube formation assay. The results revealed that COFs-derived PM2.5 exposure reduced HUVECs viability, increased the intracellular and mitochondrial ROS levels in cells, and up-regulated the levels of proteins and mRNA involved in NLRP3 inflammasome signaling pathway. However, the protein and mRNA expression of VEGF were reduced with the increasing exposure concentrations. In addition, COFs-derived PM2.5 also affected the tube formation. However, co-incubation with NAC effectively rescued the damages caused by COFs-derived PM2.5 exposure. This study proved that COFs-derived PM2.5 could significantly reduce HUVECs viability, induce the overproduction of ROS, lead to inflammation and inhibit VEGF expression, thus affect angiogenesis of HUVECs in vitro. It was revealed that the impact caused by COFs-derived PM2.5 on blood vessel formation through a ROS-mediated NLRP3 inflammasome pathway. [Display omitted] •COFs-PM2.5 exposure induces NLRP3 inflammasome activation in HUVECs.•COFs-PM2.5 exposure inhibits tube formation in HUVECs.•ROS mediates COFs-PM2.5-induced NLRP3 activation and tube formation in HUVECs.
doi_str_mv 10.1016/j.ecoenv.2019.03.028
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In our previous research, exposure to COFs-derived PM2.5 could cause umbilical vascular endothelial dysfunction, leading to decreased fetal weight. Here, to test the role of ROS-mediated NLRP3 inflammasome pathway in blood vessel formation of human umbilical vein endothelial cells (HUVECs) caused by COFs-derived PM2.5, the cells were exposed to COFs-derived PM2.5 at different concentrations with and without N-acetyl-L-cysteine (NAC). MTT assay was used to determine HUVECs viability. Intracellular ROS and mitochondrial ROS levels were assessed with DCFH-DA and MitoSOX™ assay. The levels of proteins and mRNA involved in NLRP3 inflammasome signaling pathway and VEGF were measured by western blot and real-time PCR (RT-PCR). Tube formation in HUVECs was detected by tube formation assay. The results revealed that COFs-derived PM2.5 exposure reduced HUVECs viability, increased the intracellular and mitochondrial ROS levels in cells, and up-regulated the levels of proteins and mRNA involved in NLRP3 inflammasome signaling pathway. However, the protein and mRNA expression of VEGF were reduced with the increasing exposure concentrations. In addition, COFs-derived PM2.5 also affected the tube formation. However, co-incubation with NAC effectively rescued the damages caused by COFs-derived PM2.5 exposure. This study proved that COFs-derived PM2.5 could significantly reduce HUVECs viability, induce the overproduction of ROS, lead to inflammation and inhibit VEGF expression, thus affect angiogenesis of HUVECs in vitro. It was revealed that the impact caused by COFs-derived PM2.5 on blood vessel formation through a ROS-mediated NLRP3 inflammasome pathway. 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[Display omitted] •COFs-PM2.5 exposure induces NLRP3 inflammasome activation in HUVECs.•COFs-PM2.5 exposure inhibits tube formation in HUVECs.•ROS mediates COFs-PM2.5-induced NLRP3 activation and tube formation in HUVECs.</description><subject>COFs-derived PM2.5</subject><subject>HUVECs</subject><subject>NLRP3</subject><subject>Tube formation</subject><subject>VEGF</subject><issn>0147-6513</issn><issn>1090-2414</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNp9kc2O0zAUhSMEEmXgDVh4ySbh-i9pN0hoxJ9UmNEwrC3Hvp642HGxk6J5HZ4UV2XNytKnc45sf03zmkJHgfZvDx2ahPOpY0B3HfAO2PZJs6Gwg5YJKp42G6BiaHtJ-fPmRSkHAOAg5ab5cz8hQefQLIUkR0xKP_38QJIPxK0RS2sx-xNacvuVdZKkmYwhJUtOWArWTMpRL77iZcppfZjI3c33NqL1eqmlb_u7W0787IKOUZcUkRz1Mv3WjxWSaY16JmscffBGh7pZIc42LRMGX4HBEMrL5pnToeCrf-dV8-Pjh_vrz-3-5tOX6_f71nDolxbH3hh0oreC4zDKng9SCCOHEbYIjJutkJYJw5gcpRwGIxxYg1SMI5hK-FXz5rJ7zOnXimVR0ZfzDfSMaS2K0R2nfT_Qc1RcoianUjI6dcw-6vyoKKizEnVQFyXqrEQBV1VJrb271LA-4-Qxq2I8zqb-Vq4ClE3-_wN_Adi8mS8</recordid><startdate>20190615</startdate><enddate>20190615</enddate><creator>Shen, Chaowei</creator><creator>Liu, Jie</creator><creator>Zhu, Furong</creator><creator>Lei, Ruoqian</creator><creator>Cheng, Han</creator><creator>Zhang, Chao</creator><creator>Sui, Xinmiao</creator><creator>Ding, Liu</creator><creator>Yang, Mei</creator><creator>Chen, Hongbo</creator><creator>Ding, Rui</creator><creator>Cao, Jiyu</creator><general>Elsevier Inc</general><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20190615</creationdate><title>The effects of cooking oil fumes-derived PM2.5 on blood vessel formation through ROS-mediated NLRP3 inflammasome pathway in human umbilical vein endothelial cells</title><author>Shen, Chaowei ; Liu, Jie ; Zhu, Furong ; Lei, Ruoqian ; Cheng, Han ; Zhang, Chao ; Sui, Xinmiao ; Ding, Liu ; Yang, Mei ; Chen, Hongbo ; Ding, Rui ; Cao, Jiyu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c306t-eb6ccef46d43e7b5637544c57b08e023c845d24c225b5577c4f0dce14bb0cb553</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>COFs-derived PM2.5</topic><topic>HUVECs</topic><topic>NLRP3</topic><topic>Tube formation</topic><topic>VEGF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shen, Chaowei</creatorcontrib><creatorcontrib>Liu, Jie</creatorcontrib><creatorcontrib>Zhu, Furong</creatorcontrib><creatorcontrib>Lei, Ruoqian</creatorcontrib><creatorcontrib>Cheng, Han</creatorcontrib><creatorcontrib>Zhang, Chao</creatorcontrib><creatorcontrib>Sui, Xinmiao</creatorcontrib><creatorcontrib>Ding, Liu</creatorcontrib><creatorcontrib>Yang, Mei</creatorcontrib><creatorcontrib>Chen, Hongbo</creatorcontrib><creatorcontrib>Ding, Rui</creatorcontrib><creatorcontrib>Cao, Jiyu</creatorcontrib><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Ecotoxicology and environmental safety</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shen, Chaowei</au><au>Liu, Jie</au><au>Zhu, Furong</au><au>Lei, Ruoqian</au><au>Cheng, Han</au><au>Zhang, Chao</au><au>Sui, Xinmiao</au><au>Ding, Liu</au><au>Yang, Mei</au><au>Chen, Hongbo</au><au>Ding, Rui</au><au>Cao, Jiyu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The effects of cooking oil fumes-derived PM2.5 on blood vessel formation through ROS-mediated NLRP3 inflammasome pathway in human umbilical vein endothelial cells</atitle><jtitle>Ecotoxicology and environmental safety</jtitle><date>2019-06-15</date><risdate>2019</risdate><volume>174</volume><spage>690</spage><epage>698</epage><pages>690-698</pages><issn>0147-6513</issn><eissn>1090-2414</eissn><abstract>Cooking oil fumes (COFs), a main pollutant in kitchen air, is a major risk to human health. In our previous research, exposure to COFs-derived PM2.5 could cause umbilical vascular endothelial dysfunction, leading to decreased fetal weight. Here, to test the role of ROS-mediated NLRP3 inflammasome pathway in blood vessel formation of human umbilical vein endothelial cells (HUVECs) caused by COFs-derived PM2.5, the cells were exposed to COFs-derived PM2.5 at different concentrations with and without N-acetyl-L-cysteine (NAC). MTT assay was used to determine HUVECs viability. Intracellular ROS and mitochondrial ROS levels were assessed with DCFH-DA and MitoSOX™ assay. The levels of proteins and mRNA involved in NLRP3 inflammasome signaling pathway and VEGF were measured by western blot and real-time PCR (RT-PCR). Tube formation in HUVECs was detected by tube formation assay. The results revealed that COFs-derived PM2.5 exposure reduced HUVECs viability, increased the intracellular and mitochondrial ROS levels in cells, and up-regulated the levels of proteins and mRNA involved in NLRP3 inflammasome signaling pathway. However, the protein and mRNA expression of VEGF were reduced with the increasing exposure concentrations. In addition, COFs-derived PM2.5 also affected the tube formation. However, co-incubation with NAC effectively rescued the damages caused by COFs-derived PM2.5 exposure. This study proved that COFs-derived PM2.5 could significantly reduce HUVECs viability, induce the overproduction of ROS, lead to inflammation and inhibit VEGF expression, thus affect angiogenesis of HUVECs in vitro. It was revealed that the impact caused by COFs-derived PM2.5 on blood vessel formation through a ROS-mediated NLRP3 inflammasome pathway. [Display omitted] •COFs-PM2.5 exposure induces NLRP3 inflammasome activation in HUVECs.•COFs-PM2.5 exposure inhibits tube formation in HUVECs.•ROS mediates COFs-PM2.5-induced NLRP3 activation and tube formation in HUVECs.</abstract><pub>Elsevier Inc</pub><doi>10.1016/j.ecoenv.2019.03.028</doi><tpages>9</tpages></addata></record>
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subjects COFs-derived PM2.5
HUVECs
NLRP3
Tube formation
VEGF
title The effects of cooking oil fumes-derived PM2.5 on blood vessel formation through ROS-mediated NLRP3 inflammasome pathway in human umbilical vein endothelial cells
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