Aspirin inhibits monocyte chemoattractant protein-1 and interleukin-8 expression in TNF-α stimulated human umbilical vein endothelial cells
Atherosclerosis and its complications such as stroke, myocardial infraction and peripheral vascular disease, remain the major causes of morbidity and mortality in the world. Studies have showed that chemokines and adhesion molecules are involved in causing atherosclerosis by promoting directed migra...
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description | Atherosclerosis and its complications such as stroke, myocardial infraction and peripheral vascular disease, remain the major causes of morbidity and mortality in the world. Studies have showed that chemokines and adhesion molecules are involved in causing atherosclerosis by promoting directed migration of inflammatory cells. Monocyte chemoattractant protein-1 (MCP-1) is one of the key factors critical for the initiating and developing of atherosclerotic lesions. IL-8, a CXC chemokine, stimulates neutrophil chemotaxis. Aspirin is the most common drug used to prevent the complications of atherosclerosis such as stroke and coronary heart disease. In this study, we found that aspirin inhibited TNF-α (10
ng/ml)-induced MCP-1 and IL-8 expression at the RNA and protein levels in human umbilical vein endothelial cells (HUVECs), monocyte adhesion and transmigration, and that its inhibitory effects were not due to decreased HUVEC viability as assessed by MTT test. Aspirin at the dose as low as 10
μg/ml significantly inhibited the release of TNF-stimulated MCP-1 by 29.1% (
P=0.008) and IL-8 by 26.9% (
P=0.0146) as compared to TNF-stimulated release. Antibodies pretreatment were likely to decrease the production of MCP-1 (
P |
doi_str_mv | 10.1016/j.atherosclerosis.2004.01.024 |
format | Article |
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ng/ml)-induced MCP-1 and IL-8 expression at the RNA and protein levels in human umbilical vein endothelial cells (HUVECs), monocyte adhesion and transmigration, and that its inhibitory effects were not due to decreased HUVEC viability as assessed by MTT test. Aspirin at the dose as low as 10
μg/ml significantly inhibited the release of TNF-stimulated MCP-1 by 29.1% (
P=0.008) and IL-8 by 26.9% (
P=0.0146) as compared to TNF-stimulated release. Antibodies pretreatment were likely to decrease the production of MCP-1 (
P<0.0001) and IL-8 (
P<0.0001). Furthermore, aspirin (10
μg/ml) inhibited U937 cell adhesion by a 13.4% (
P=0.0119) inhibition as compared to TNF-stimulated alone. Finally, at higher concentration, aspirin also inhibited U937 migration to HUVEC by 89.1% (
P=0.0475) as compared to TNF-stimulated alone. These results in our study suggest that aspirin inhibits TNF-α stimulated MCP-1 and IL-8 release in HUVECs, for its additional therapeutic effects of aspirin in causing atherosclerosis.</description><identifier>ISSN: 0021-9150</identifier><identifier>EISSN: 1879-1484</identifier><identifier>DOI: 10.1016/j.atherosclerosis.2004.01.024</identifier><identifier>PMID: 15136050</identifier><language>eng</language><publisher>Amsterdam: Elsevier Ireland Ltd</publisher><subject>Animals ; Arteriosclerosis - prevention & control ; Aspirin ; Aspirin - pharmacology ; Atherosclerosis ; Atherosclerosis (general aspects, experimental research) ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Cell Adhesion - drug effects ; Cell Movement - physiology ; Cells, Cultured ; Chemokine CCL2 - genetics ; Chemokine CCL2 - metabolism ; Endothelial Cells - drug effects ; Endothelial Cells - metabolism ; Human vascular endothelial cell ; Humans ; IL-8 ; Interleukin-8 - genetics ; Interleukin-8 - metabolism ; Medical sciences ; Monocyte chemoattractant protein-1 ; Probability ; Reverse Transcriptase Polymerase Chain Reaction - methods ; RNA, Messenger - analysis ; Sensitivity and Specificity ; Tumor Necrosis Factor-alpha - antagonists & inhibitors ; Umbilical Veins - cytology</subject><ispartof>Atherosclerosis, 2004-06, Vol.174 (2), p.207-213</ispartof><rights>2004 Elsevier Ireland Ltd</rights><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c415t-4d3072bcf7580bd0924a424415bf1f403fbc3f6b897a3c6171ab8f4967f054963</citedby><cites>FETCH-LOGICAL-c415t-4d3072bcf7580bd0924a424415bf1f403fbc3f6b897a3c6171ab8f4967f054963</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S002191500400084X$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27903,27904,65309</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15767668$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15136050$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yang, Yi-Yuan</creatorcontrib><creatorcontrib>Hu, Chaur-Jong</creatorcontrib><creatorcontrib>Chang, Su-Mei</creatorcontrib><creatorcontrib>Tai, Tzu-Yi</creatorcontrib><creatorcontrib>Leu, Sy-Jye</creatorcontrib><title>Aspirin inhibits monocyte chemoattractant protein-1 and interleukin-8 expression in TNF-α stimulated human umbilical vein endothelial cells</title><title>Atherosclerosis</title><addtitle>Atherosclerosis</addtitle><description>Atherosclerosis and its complications such as stroke, myocardial infraction and peripheral vascular disease, remain the major causes of morbidity and mortality in the world. Studies have showed that chemokines and adhesion molecules are involved in causing atherosclerosis by promoting directed migration of inflammatory cells. Monocyte chemoattractant protein-1 (MCP-1) is one of the key factors critical for the initiating and developing of atherosclerotic lesions. IL-8, a CXC chemokine, stimulates neutrophil chemotaxis. Aspirin is the most common drug used to prevent the complications of atherosclerosis such as stroke and coronary heart disease. In this study, we found that aspirin inhibited TNF-α (10
ng/ml)-induced MCP-1 and IL-8 expression at the RNA and protein levels in human umbilical vein endothelial cells (HUVECs), monocyte adhesion and transmigration, and that its inhibitory effects were not due to decreased HUVEC viability as assessed by MTT test. Aspirin at the dose as low as 10
μg/ml significantly inhibited the release of TNF-stimulated MCP-1 by 29.1% (
P=0.008) and IL-8 by 26.9% (
P=0.0146) as compared to TNF-stimulated release. Antibodies pretreatment were likely to decrease the production of MCP-1 (
P<0.0001) and IL-8 (
P<0.0001). Furthermore, aspirin (10
μg/ml) inhibited U937 cell adhesion by a 13.4% (
P=0.0119) inhibition as compared to TNF-stimulated alone. Finally, at higher concentration, aspirin also inhibited U937 migration to HUVEC by 89.1% (
P=0.0475) as compared to TNF-stimulated alone. These results in our study suggest that aspirin inhibits TNF-α stimulated MCP-1 and IL-8 release in HUVECs, for its additional therapeutic effects of aspirin in causing atherosclerosis.</description><subject>Animals</subject><subject>Arteriosclerosis - prevention & control</subject><subject>Aspirin</subject><subject>Aspirin - pharmacology</subject><subject>Atherosclerosis</subject><subject>Atherosclerosis (general aspects, experimental research)</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Cell Adhesion - drug effects</subject><subject>Cell Movement - physiology</subject><subject>Cells, Cultured</subject><subject>Chemokine CCL2 - genetics</subject><subject>Chemokine CCL2 - metabolism</subject><subject>Endothelial Cells - drug effects</subject><subject>Endothelial Cells - metabolism</subject><subject>Human vascular endothelial cell</subject><subject>Humans</subject><subject>IL-8</subject><subject>Interleukin-8 - genetics</subject><subject>Interleukin-8 - metabolism</subject><subject>Medical sciences</subject><subject>Monocyte chemoattractant protein-1</subject><subject>Probability</subject><subject>Reverse Transcriptase Polymerase Chain Reaction - methods</subject><subject>RNA, Messenger - analysis</subject><subject>Sensitivity and Specificity</subject><subject>Tumor Necrosis Factor-alpha - antagonists & inhibitors</subject><subject>Umbilical Veins - cytology</subject><issn>0021-9150</issn><issn>1879-1484</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkcFu1DAQhi0EotvCKyBfyi1hJnHi5MChqmiLVMGlnC3HGWu9JM5iOxV9B16GF-GZ8GpXqsSJi0eyv_k98_-MXSKUCNh-2JU6bSks0UyH08WyAhAlYAmVeME22Mm-QNGJl2wDUGHRYwNn7DzGHWRQYveanWGDdQsNbNivq7h3wXnu_NYNLkU-L34xT4m42dK86JSCNkn7xPdhSeR8gVz7MfOJwkTr93zTcfq5DxSjWw5C_OHLTfHnN4_JzeukE418u87a83Ue3OSMnvhjFuLkxyXvMrl8YWia4hv2yuop0ttTvWDfbj49XN8V919vP19f3RdGYJMKMdYgq8FY2XQwjNBXQotK5LfBohVQ28HUth26XuratChRD50VfSstNLnUF-z9UTev9GOlmNTs4mEC7WlZo5LYY50NyuDHI2iy1TGQVfvgZh2eFII6xKF26p841CEOBahyHLn_3emjdZhpfO4--Z-ByxOgY_bFBu1N1njmZCvbtsvc7ZGjbMujo6CiceQNjS6QSWpc3H-O9BdceLYn</recordid><startdate>20040601</startdate><enddate>20040601</enddate><creator>Yang, Yi-Yuan</creator><creator>Hu, Chaur-Jong</creator><creator>Chang, Su-Mei</creator><creator>Tai, Tzu-Yi</creator><creator>Leu, Sy-Jye</creator><general>Elsevier Ireland Ltd</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20040601</creationdate><title>Aspirin inhibits monocyte chemoattractant protein-1 and interleukin-8 expression in TNF-α stimulated human umbilical vein endothelial cells</title><author>Yang, Yi-Yuan ; Hu, Chaur-Jong ; Chang, Su-Mei ; Tai, Tzu-Yi ; Leu, Sy-Jye</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c415t-4d3072bcf7580bd0924a424415bf1f403fbc3f6b897a3c6171ab8f4967f054963</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Arteriosclerosis - prevention & control</topic><topic>Aspirin</topic><topic>Aspirin - pharmacology</topic><topic>Atherosclerosis</topic><topic>Atherosclerosis (general aspects, experimental research)</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Cell Adhesion - drug effects</topic><topic>Cell Movement - physiology</topic><topic>Cells, Cultured</topic><topic>Chemokine CCL2 - genetics</topic><topic>Chemokine CCL2 - metabolism</topic><topic>Endothelial Cells - drug effects</topic><topic>Endothelial Cells - metabolism</topic><topic>Human vascular endothelial cell</topic><topic>Humans</topic><topic>IL-8</topic><topic>Interleukin-8 - genetics</topic><topic>Interleukin-8 - metabolism</topic><topic>Medical sciences</topic><topic>Monocyte chemoattractant protein-1</topic><topic>Probability</topic><topic>Reverse Transcriptase Polymerase Chain Reaction - methods</topic><topic>RNA, Messenger - analysis</topic><topic>Sensitivity and Specificity</topic><topic>Tumor Necrosis Factor-alpha - antagonists & inhibitors</topic><topic>Umbilical Veins - cytology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yang, Yi-Yuan</creatorcontrib><creatorcontrib>Hu, Chaur-Jong</creatorcontrib><creatorcontrib>Chang, Su-Mei</creatorcontrib><creatorcontrib>Tai, Tzu-Yi</creatorcontrib><creatorcontrib>Leu, Sy-Jye</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Atherosclerosis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, Yi-Yuan</au><au>Hu, Chaur-Jong</au><au>Chang, Su-Mei</au><au>Tai, Tzu-Yi</au><au>Leu, Sy-Jye</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Aspirin inhibits monocyte chemoattractant protein-1 and interleukin-8 expression in TNF-α stimulated human umbilical vein endothelial cells</atitle><jtitle>Atherosclerosis</jtitle><addtitle>Atherosclerosis</addtitle><date>2004-06-01</date><risdate>2004</risdate><volume>174</volume><issue>2</issue><spage>207</spage><epage>213</epage><pages>207-213</pages><issn>0021-9150</issn><eissn>1879-1484</eissn><abstract>Atherosclerosis and its complications such as stroke, myocardial infraction and peripheral vascular disease, remain the major causes of morbidity and mortality in the world. Studies have showed that chemokines and adhesion molecules are involved in causing atherosclerosis by promoting directed migration of inflammatory cells. Monocyte chemoattractant protein-1 (MCP-1) is one of the key factors critical for the initiating and developing of atherosclerotic lesions. IL-8, a CXC chemokine, stimulates neutrophil chemotaxis. Aspirin is the most common drug used to prevent the complications of atherosclerosis such as stroke and coronary heart disease. In this study, we found that aspirin inhibited TNF-α (10
ng/ml)-induced MCP-1 and IL-8 expression at the RNA and protein levels in human umbilical vein endothelial cells (HUVECs), monocyte adhesion and transmigration, and that its inhibitory effects were not due to decreased HUVEC viability as assessed by MTT test. Aspirin at the dose as low as 10
μg/ml significantly inhibited the release of TNF-stimulated MCP-1 by 29.1% (
P=0.008) and IL-8 by 26.9% (
P=0.0146) as compared to TNF-stimulated release. Antibodies pretreatment were likely to decrease the production of MCP-1 (
P<0.0001) and IL-8 (
P<0.0001). Furthermore, aspirin (10
μg/ml) inhibited U937 cell adhesion by a 13.4% (
P=0.0119) inhibition as compared to TNF-stimulated alone. Finally, at higher concentration, aspirin also inhibited U937 migration to HUVEC by 89.1% (
P=0.0475) as compared to TNF-stimulated alone. These results in our study suggest that aspirin inhibits TNF-α stimulated MCP-1 and IL-8 release in HUVECs, for its additional therapeutic effects of aspirin in causing atherosclerosis.</abstract><cop>Amsterdam</cop><pub>Elsevier Ireland Ltd</pub><pmid>15136050</pmid><doi>10.1016/j.atherosclerosis.2004.01.024</doi><tpages>7</tpages></addata></record> |
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subjects | Animals Arteriosclerosis - prevention & control Aspirin Aspirin - pharmacology Atherosclerosis Atherosclerosis (general aspects, experimental research) Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Cell Adhesion - drug effects Cell Movement - physiology Cells, Cultured Chemokine CCL2 - genetics Chemokine CCL2 - metabolism Endothelial Cells - drug effects Endothelial Cells - metabolism Human vascular endothelial cell Humans IL-8 Interleukin-8 - genetics Interleukin-8 - metabolism Medical sciences Monocyte chemoattractant protein-1 Probability Reverse Transcriptase Polymerase Chain Reaction - methods RNA, Messenger - analysis Sensitivity and Specificity Tumor Necrosis Factor-alpha - antagonists & inhibitors Umbilical Veins - cytology |
title | Aspirin inhibits monocyte chemoattractant protein-1 and interleukin-8 expression in TNF-α stimulated human umbilical vein endothelial cells |
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