Glucose Regulates Monocyte Adhesion Through Endothelial Production of Interleukin-8
ABSTRACT—We have shown that glucose increases monocyte adhesion to human aortic endothelial cells (HAECs) in vitro. In the present study, we examined mechanisms by which glucose stimulates monocyte:endothelial interactions. HAECs cultured for 7 days in 25 mmol/L glucose had a 2-fold elevation in int...
Gespeichert in:
| Veröffentlicht in: | Circulation research 2003-03, Vol.92 (4), p.371-377 |
|---|---|
| Hauptverfasser: | , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 377 |
|---|---|
| container_issue | 4 |
| container_start_page | 371 |
| container_title | Circulation research |
| container_volume | 92 |
| creator | Srinivasan, Suseela Yeh, Michael Danziger, Eric C Hatley, Melissa E Riggan, Anna E Leitinger, Norbert Berliner, Judith A Hedrick, Catherine C |
| description | ABSTRACT—We have shown that glucose increases monocyte adhesion to human aortic endothelial cells (HAECs) in vitro. In the present study, we examined mechanisms by which glucose stimulates monocyte:endothelial interactions. HAECs cultured for 7 days in 25 mmol/L glucose had a 2-fold elevation in interleukin-8 (IL-8) secretion over control cells cultured in 5.5 mmol/L glucose (P |
| doi_str_mv | 10.1161/01.RES.0000061714.74668.5C |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_73091335</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>73091335</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5717-19323ba5921d1156a6d195fa84ca00ed62a62e7af19347e46236a5be7e286943</originalsourceid><addsrcrecordid>eNpdkNtq3DAQQEVpabZpf6GYQPtmV6Or3bewbNNASkuy70Jrj2MnWiuVLEL-vnJ2YaHzMjBz5sIh5AJoBaDgG4XqdnNX0SUUaBCVFkrVlVy_ISuQTJRCanhLVrnflJpzekY-xPhAKQjOmvfkDJiitNb1itxdudT6iMUt3idnZ4zFLz_59mXG4rIbMI5-KrZD8Ol-KDZT5-cB3Whd8Sf4LrXz0vZ9cT3NGBymx3Eq64_kXW9dxE_HfE62Pzbb9c_y5vfV9frypmzze7qEhjO-s7Jh0AFIZVUHjextLVpLKXaKWcVQ2z6DQqNQjCsrd6iR1aoR_Jx8Pax9Cv5vwjib_RhbdM5O6FM0mtMGOJcZvPgPfPApTPk1w4AJVtd0gb4foDb4GAP25imMexteDFCzaDcUTNZuTtrNq3Yj13n48_FC2u2xO40ePWfgyxGwsbWuD3Zqx3jihAKlOM2cOHDP3mWj8dGlZwxmQOvm4fU0p8BKtmRONS2Xkub_AHJAmWk</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>212428805</pqid></control><display><type>article</type><title>Glucose Regulates Monocyte Adhesion Through Endothelial Production of Interleukin-8</title><source>Journals@Ovid Ovid Autoload</source><source>MEDLINE</source><source>American Heart Association Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><creator>Srinivasan, Suseela ; Yeh, Michael ; Danziger, Eric C ; Hatley, Melissa E ; Riggan, Anna E ; Leitinger, Norbert ; Berliner, Judith A ; Hedrick, Catherine C</creator><creatorcontrib>Srinivasan, Suseela ; Yeh, Michael ; Danziger, Eric C ; Hatley, Melissa E ; Riggan, Anna E ; Leitinger, Norbert ; Berliner, Judith A ; Hedrick, Catherine C</creatorcontrib><description>ABSTRACT—We have shown that glucose increases monocyte adhesion to human aortic endothelial cells (HAECs) in vitro. In the present study, we examined mechanisms by which glucose stimulates monocyte:endothelial interactions. HAECs cultured for 7 days in 25 mmol/L glucose had a 2-fold elevation in interleukin-8 (IL-8) secretion over control cells cultured in 5.5 mmol/L glucose (P <0.001). Use of a neutralizing antibody to IL-8 prevented glucose-mediated monocyte adhesion. Both glucose and IL-8 activated β1 integrin on the HAEC surface, suggesting that both activate the α5β1 integrin complex on the endothelial surface. The α5β1 integrin complex is important for anchoring connecting segment-1 fibronectin on the HAEC surface for monocyte adhesion. Analysis of the human IL-8 promoter revealed binding sites for NF-κB and AP-1 as well as several aligned carbohydrate response elements (also known as E-boxes). Glucose dramatically stimulated IL-8 promoter activity. Using mutated IL-8 promoter constructs and EMSA, we found that the AP-1 element and the glucose-response element were responsible for much of the glucose-mediated activation of IL-8 transcription. Interestingly, inhibition of reactive oxygen species (ROS) production through use of pharmacological uncouplers of the mitochondrial electron transport chain significantly reduced glucose-mediated induction of IL-8 expression. These data indicate that glucose regulates monocyte:endothelial interactions through stimulation of IL-8 and ROS production and activation of the α5β1 integrin complex on HAECs.</description><identifier>ISSN: 0009-7330</identifier><identifier>EISSN: 1524-4571</identifier><identifier>DOI: 10.1161/01.RES.0000061714.74668.5C</identifier><identifier>PMID: 12600878</identifier><identifier>CODEN: CIRUAL</identifier><language>eng</language><publisher>Hagerstown, MD: American Heart Association, Inc</publisher><subject>Animals ; Associated diseases and complications ; Binding Sites - genetics ; Biological and medical sciences ; Carbonyl Cyanide m-Chlorophenyl Hydrazone - pharmacology ; Cell Adhesion - drug effects ; Cell Adhesion - physiology ; Cells, Cultured ; Diabetes Mellitus, Type 2 - physiopathology ; Diabetes. Impaired glucose tolerance ; Dose-Response Relationship, Drug ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Endothelium, Vascular - cytology ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - metabolism ; Gene Expression Regulation - drug effects ; Glucose - pharmacology ; Humans ; Interleukin-8 - biosynthesis ; Interleukin-8 - genetics ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Mitochondria - drug effects ; Mitochondria - metabolism ; Monocytes - cytology ; Monocytes - drug effects ; Promoter Regions, Genetic - genetics ; Reactive Oxygen Species - metabolism ; RNA, Messenger - drug effects ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Thenoyltrifluoroacetone - pharmacology ; Transcription Factor AP-1 - metabolism ; Uncoupling Agents - pharmacology</subject><ispartof>Circulation research, 2003-03, Vol.92 (4), p.371-377</ispartof><rights>2003 American Heart Association, Inc.</rights><rights>2003 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Mar 7 2003</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5717-19323ba5921d1156a6d195fa84ca00ed62a62e7af19347e46236a5be7e286943</citedby><cites>FETCH-LOGICAL-c5717-19323ba5921d1156a6d195fa84ca00ed62a62e7af19347e46236a5be7e286943</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3674,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14616630$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12600878$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Srinivasan, Suseela</creatorcontrib><creatorcontrib>Yeh, Michael</creatorcontrib><creatorcontrib>Danziger, Eric C</creatorcontrib><creatorcontrib>Hatley, Melissa E</creatorcontrib><creatorcontrib>Riggan, Anna E</creatorcontrib><creatorcontrib>Leitinger, Norbert</creatorcontrib><creatorcontrib>Berliner, Judith A</creatorcontrib><creatorcontrib>Hedrick, Catherine C</creatorcontrib><title>Glucose Regulates Monocyte Adhesion Through Endothelial Production of Interleukin-8</title><title>Circulation research</title><addtitle>Circ Res</addtitle><description>ABSTRACT—We have shown that glucose increases monocyte adhesion to human aortic endothelial cells (HAECs) in vitro. In the present study, we examined mechanisms by which glucose stimulates monocyte:endothelial interactions. HAECs cultured for 7 days in 25 mmol/L glucose had a 2-fold elevation in interleukin-8 (IL-8) secretion over control cells cultured in 5.5 mmol/L glucose (P <0.001). Use of a neutralizing antibody to IL-8 prevented glucose-mediated monocyte adhesion. Both glucose and IL-8 activated β1 integrin on the HAEC surface, suggesting that both activate the α5β1 integrin complex on the endothelial surface. The α5β1 integrin complex is important for anchoring connecting segment-1 fibronectin on the HAEC surface for monocyte adhesion. Analysis of the human IL-8 promoter revealed binding sites for NF-κB and AP-1 as well as several aligned carbohydrate response elements (also known as E-boxes). Glucose dramatically stimulated IL-8 promoter activity. Using mutated IL-8 promoter constructs and EMSA, we found that the AP-1 element and the glucose-response element were responsible for much of the glucose-mediated activation of IL-8 transcription. Interestingly, inhibition of reactive oxygen species (ROS) production through use of pharmacological uncouplers of the mitochondrial electron transport chain significantly reduced glucose-mediated induction of IL-8 expression. These data indicate that glucose regulates monocyte:endothelial interactions through stimulation of IL-8 and ROS production and activation of the α5β1 integrin complex on HAECs.</description><subject>Animals</subject><subject>Associated diseases and complications</subject><subject>Binding Sites - genetics</subject><subject>Biological and medical sciences</subject><subject>Carbonyl Cyanide m-Chlorophenyl Hydrazone - pharmacology</subject><subject>Cell Adhesion - drug effects</subject><subject>Cell Adhesion - physiology</subject><subject>Cells, Cultured</subject><subject>Diabetes Mellitus, Type 2 - physiopathology</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Dose-Response Relationship, Drug</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Endothelium, Vascular - cytology</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Glucose - pharmacology</subject><subject>Humans</subject><subject>Interleukin-8 - biosynthesis</subject><subject>Interleukin-8 - genetics</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Obese</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - metabolism</subject><subject>Monocytes - cytology</subject><subject>Monocytes - drug effects</subject><subject>Promoter Regions, Genetic - genetics</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>RNA, Messenger - drug effects</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Thenoyltrifluoroacetone - pharmacology</subject><subject>Transcription Factor AP-1 - metabolism</subject><subject>Uncoupling Agents - pharmacology</subject><issn>0009-7330</issn><issn>1524-4571</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkNtq3DAQQEVpabZpf6GYQPtmV6Or3bewbNNASkuy70Jrj2MnWiuVLEL-vnJ2YaHzMjBz5sIh5AJoBaDgG4XqdnNX0SUUaBCVFkrVlVy_ISuQTJRCanhLVrnflJpzekY-xPhAKQjOmvfkDJiitNb1itxdudT6iMUt3idnZ4zFLz_59mXG4rIbMI5-KrZD8Ol-KDZT5-cB3Whd8Sf4LrXz0vZ9cT3NGBymx3Eq64_kXW9dxE_HfE62Pzbb9c_y5vfV9frypmzze7qEhjO-s7Jh0AFIZVUHjextLVpLKXaKWcVQ2z6DQqNQjCsrd6iR1aoR_Jx8Pax9Cv5vwjib_RhbdM5O6FM0mtMGOJcZvPgPfPApTPk1w4AJVtd0gb4foDb4GAP25imMexteDFCzaDcUTNZuTtrNq3Yj13n48_FC2u2xO40ePWfgyxGwsbWuD3Zqx3jihAKlOM2cOHDP3mWj8dGlZwxmQOvm4fU0p8BKtmRONS2Xkub_AHJAmWk</recordid><startdate>20030307</startdate><enddate>20030307</enddate><creator>Srinivasan, Suseela</creator><creator>Yeh, Michael</creator><creator>Danziger, Eric C</creator><creator>Hatley, Melissa E</creator><creator>Riggan, Anna E</creator><creator>Leitinger, Norbert</creator><creator>Berliner, Judith A</creator><creator>Hedrick, Catherine C</creator><general>American Heart Association, Inc</general><general>Lippincott</general><general>Lippincott Williams & Wilkins Ovid Technologies</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>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>20030307</creationdate><title>Glucose Regulates Monocyte Adhesion Through Endothelial Production of Interleukin-8</title><author>Srinivasan, Suseela ; Yeh, Michael ; Danziger, Eric C ; Hatley, Melissa E ; Riggan, Anna E ; Leitinger, Norbert ; Berliner, Judith A ; Hedrick, Catherine C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5717-19323ba5921d1156a6d195fa84ca00ed62a62e7af19347e46236a5be7e286943</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Associated diseases and complications</topic><topic>Binding Sites - genetics</topic><topic>Biological and medical sciences</topic><topic>Carbonyl Cyanide m-Chlorophenyl Hydrazone - pharmacology</topic><topic>Cell Adhesion - drug effects</topic><topic>Cell Adhesion - physiology</topic><topic>Cells, Cultured</topic><topic>Diabetes Mellitus, Type 2 - physiopathology</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Dose-Response Relationship, Drug</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Endothelium, Vascular - cytology</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Glucose - pharmacology</topic><topic>Humans</topic><topic>Interleukin-8 - biosynthesis</topic><topic>Interleukin-8 - genetics</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Obese</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - metabolism</topic><topic>Monocytes - cytology</topic><topic>Monocytes - drug effects</topic><topic>Promoter Regions, Genetic - genetics</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>RNA, Messenger - drug effects</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Thenoyltrifluoroacetone - pharmacology</topic><topic>Transcription Factor AP-1 - metabolism</topic><topic>Uncoupling Agents - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Srinivasan, Suseela</creatorcontrib><creatorcontrib>Yeh, Michael</creatorcontrib><creatorcontrib>Danziger, Eric C</creatorcontrib><creatorcontrib>Hatley, Melissa E</creatorcontrib><creatorcontrib>Riggan, Anna E</creatorcontrib><creatorcontrib>Leitinger, Norbert</creatorcontrib><creatorcontrib>Berliner, Judith A</creatorcontrib><creatorcontrib>Hedrick, Catherine C</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>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Srinivasan, Suseela</au><au>Yeh, Michael</au><au>Danziger, Eric C</au><au>Hatley, Melissa E</au><au>Riggan, Anna E</au><au>Leitinger, Norbert</au><au>Berliner, Judith A</au><au>Hedrick, Catherine C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Glucose Regulates Monocyte Adhesion Through Endothelial Production of Interleukin-8</atitle><jtitle>Circulation research</jtitle><addtitle>Circ Res</addtitle><date>2003-03-07</date><risdate>2003</risdate><volume>92</volume><issue>4</issue><spage>371</spage><epage>377</epage><pages>371-377</pages><issn>0009-7330</issn><eissn>1524-4571</eissn><coden>CIRUAL</coden><abstract>ABSTRACT—We have shown that glucose increases monocyte adhesion to human aortic endothelial cells (HAECs) in vitro. In the present study, we examined mechanisms by which glucose stimulates monocyte:endothelial interactions. HAECs cultured for 7 days in 25 mmol/L glucose had a 2-fold elevation in interleukin-8 (IL-8) secretion over control cells cultured in 5.5 mmol/L glucose (P <0.001). Use of a neutralizing antibody to IL-8 prevented glucose-mediated monocyte adhesion. Both glucose and IL-8 activated β1 integrin on the HAEC surface, suggesting that both activate the α5β1 integrin complex on the endothelial surface. The α5β1 integrin complex is important for anchoring connecting segment-1 fibronectin on the HAEC surface for monocyte adhesion. Analysis of the human IL-8 promoter revealed binding sites for NF-κB and AP-1 as well as several aligned carbohydrate response elements (also known as E-boxes). Glucose dramatically stimulated IL-8 promoter activity. Using mutated IL-8 promoter constructs and EMSA, we found that the AP-1 element and the glucose-response element were responsible for much of the glucose-mediated activation of IL-8 transcription. Interestingly, inhibition of reactive oxygen species (ROS) production through use of pharmacological uncouplers of the mitochondrial electron transport chain significantly reduced glucose-mediated induction of IL-8 expression. These data indicate that glucose regulates monocyte:endothelial interactions through stimulation of IL-8 and ROS production and activation of the α5β1 integrin complex on HAECs.</abstract><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>12600878</pmid><doi>10.1161/01.RES.0000061714.74668.5C</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0009-7330 |
| ispartof | Circulation research, 2003-03, Vol.92 (4), p.371-377 |
| issn | 0009-7330 1524-4571 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_73091335 |
| source | Journals@Ovid Ovid Autoload; MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Animals Associated diseases and complications Binding Sites - genetics Biological and medical sciences Carbonyl Cyanide m-Chlorophenyl Hydrazone - pharmacology Cell Adhesion - drug effects Cell Adhesion - physiology Cells, Cultured Diabetes Mellitus, Type 2 - physiopathology Diabetes. Impaired glucose tolerance Dose-Response Relationship, Drug Endocrine pancreas. Apud cells (diseases) Endocrinopathies Endothelium, Vascular - cytology Endothelium, Vascular - drug effects Endothelium, Vascular - metabolism Gene Expression Regulation - drug effects Glucose - pharmacology Humans Interleukin-8 - biosynthesis Interleukin-8 - genetics Medical sciences Mice Mice, Inbred C57BL Mice, Obese Mitochondria - drug effects Mitochondria - metabolism Monocytes - cytology Monocytes - drug effects Promoter Regions, Genetic - genetics Reactive Oxygen Species - metabolism RNA, Messenger - drug effects RNA, Messenger - genetics RNA, Messenger - metabolism Thenoyltrifluoroacetone - pharmacology Transcription Factor AP-1 - metabolism Uncoupling Agents - pharmacology |
| title | Glucose Regulates Monocyte Adhesion Through Endothelial Production of Interleukin-8 |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-12T14%3A24%3A09IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Glucose%20Regulates%20Monocyte%20Adhesion%20Through%20Endothelial%20Production%20of%20Interleukin-8&rft.jtitle=Circulation%20research&rft.au=Srinivasan,%20Suseela&rft.date=2003-03-07&rft.volume=92&rft.issue=4&rft.spage=371&rft.epage=377&rft.pages=371-377&rft.issn=0009-7330&rft.eissn=1524-4571&rft.coden=CIRUAL&rft_id=info:doi/10.1161/01.RES.0000061714.74668.5C&rft_dat=%3Cproquest_cross%3E73091335%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=212428805&rft_id=info:pmid/12600878&rfr_iscdi=true |