Inflammatory events in a vascular remodeling model induced by surgical injury to the rat carotid artery
The aim of our study was to gain insight into the molecular and cellular mechanisms of the inflammatory response to arterial injury in a rat experimental model. Rats (five for each experimental time) were subjected to brief clamping and longitudinal incision of a carotid artery and monitored for 30...
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| Veröffentlicht in: | British journal of pharmacology 2006-01, Vol.147 (2), p.175-182 |
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| creator | Rinaldi, Barbara Romagnoli, Paolo Bacci, Stefano Carnuccio, Rosa Maiuri, Maria Chiara Donniacuo, Maria Capuano, Annalisa Rossi, Francesco Filippelli, Amelia |
| description | The aim of our study was to gain insight into the molecular and cellular mechanisms of the inflammatory response to arterial injury in a rat experimental model.
Rats (five for each experimental time) were subjected to brief clamping and longitudinal incision of a carotid artery and monitored for 30 days. Subsequently, Nuclear Factor‐kappaB (NF‐κB) expression was measured by electrophoretic mobility shift assay. Heat shock protein (HSP) 27, HSP47 and HSP70 were evaluated by Western blot. Morphological changes of the vessel wall were investigated by light and electron microscopy.
In injured rat carotid artery NF‐κB activity started immediately upon injury, and peaked between 2 and 3 weeks later. Western blot showed a significant increase of HSP47 and HSP70 7 days after injury. At 2 weeks postinjury, HSP27 expression peaked. Ligth microscopy showed a neointima formation, discontinuity of the media layer and a rich infiltrate. Among infiltrating cells electron microscopy identified dendritic‐like cells in contact with lymphocytes.
Our model of surgical injury induces a significant inflammatory process characterized by enhanced NF‐κB activity and HSPs hyperexpression. Dendritic‐like cells were for the first time identified as a novel component of tissue repair consequent to acute arterial injury.
British Journal of Pharmacology (2006) 147, 175–182. doi:10.1038/sj.bjp.0706472 |
| doi_str_mv | 10.1038/sj.bjp.0706472 |
| format | Article |
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Rats (five for each experimental time) were subjected to brief clamping and longitudinal incision of a carotid artery and monitored for 30 days. Subsequently, Nuclear Factor‐kappaB (NF‐κB) expression was measured by electrophoretic mobility shift assay. Heat shock protein (HSP) 27, HSP47 and HSP70 were evaluated by Western blot. Morphological changes of the vessel wall were investigated by light and electron microscopy.
In injured rat carotid artery NF‐κB activity started immediately upon injury, and peaked between 2 and 3 weeks later. Western blot showed a significant increase of HSP47 and HSP70 7 days after injury. At 2 weeks postinjury, HSP27 expression peaked. Ligth microscopy showed a neointima formation, discontinuity of the media layer and a rich infiltrate. Among infiltrating cells electron microscopy identified dendritic‐like cells in contact with lymphocytes.
Our model of surgical injury induces a significant inflammatory process characterized by enhanced NF‐κB activity and HSPs hyperexpression. Dendritic‐like cells were for the first time identified as a novel component of tissue repair consequent to acute arterial injury.
British Journal of Pharmacology (2006) 147, 175–182. doi:10.1038/sj.bjp.0706472</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1038/sj.bjp.0706472</identifier><identifier>PMID: 16299548</identifier><identifier>CODEN: BJPCBM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Acute Disease ; Animals ; Biological and medical sciences ; Carotid Arteries - metabolism ; Carotid Arteries - pathology ; Carotid Arteries - ultrastructure ; Carotid Artery Injuries - etiology ; Carotid Artery Injuries - metabolism ; Carotid Artery Injuries - pathology ; carotid injury ; Endothelium, Vascular - pathology ; Endothelium, Vascular - ultrastructure ; heat shock protein ; Heat-Shock Proteins - biosynthesis ; HSP27 Heat-Shock Proteins ; HSP47 Heat-Shock Proteins - biosynthesis ; HSP70 Heat-Shock Proteins - biosynthesis ; Immunohistochemistry ; Inflammation - metabolism ; Kinetics ; Male ; Medical sciences ; Microscopy, Electron ; Neoplasm Proteins - biosynthesis ; NF-kappa B - metabolism ; Nuclear factor kappa B ; Pharmacology. Drug treatments ; Rats ; Rats, Wistar ; remodeling ; Tunica Intima - pathology ; Tunica Media - pathology ; Vascular Surgical Procedures - adverse effects</subject><ispartof>British journal of pharmacology, 2006-01, Vol.147 (2), p.175-182</ispartof><rights>2006 British Pharmacological Society</rights><rights>2006 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Jan 2006</rights><rights>Copyright 2006, Nature Publishing Group 2006 Nature Publishing Group</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4898-a0e6e0d6f819ab323ae562750ee570ac5bf1ce9d0e43ff90ef71632d545e37ce3</citedby><cites>FETCH-LOGICAL-c4898-a0e6e0d6f819ab323ae562750ee570ac5bf1ce9d0e43ff90ef71632d545e37ce3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1615853/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1615853/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,315,728,781,785,886,1418,1434,27928,27929,45578,45579,46413,46837,53795,53797</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17675039$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16299548$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rinaldi, Barbara</creatorcontrib><creatorcontrib>Romagnoli, Paolo</creatorcontrib><creatorcontrib>Bacci, Stefano</creatorcontrib><creatorcontrib>Carnuccio, Rosa</creatorcontrib><creatorcontrib>Maiuri, Maria Chiara</creatorcontrib><creatorcontrib>Donniacuo, Maria</creatorcontrib><creatorcontrib>Capuano, Annalisa</creatorcontrib><creatorcontrib>Rossi, Francesco</creatorcontrib><creatorcontrib>Filippelli, Amelia</creatorcontrib><title>Inflammatory events in a vascular remodeling model induced by surgical injury to the rat carotid artery</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>The aim of our study was to gain insight into the molecular and cellular mechanisms of the inflammatory response to arterial injury in a rat experimental model.
Rats (five for each experimental time) were subjected to brief clamping and longitudinal incision of a carotid artery and monitored for 30 days. Subsequently, Nuclear Factor‐kappaB (NF‐κB) expression was measured by electrophoretic mobility shift assay. Heat shock protein (HSP) 27, HSP47 and HSP70 were evaluated by Western blot. Morphological changes of the vessel wall were investigated by light and electron microscopy.
In injured rat carotid artery NF‐κB activity started immediately upon injury, and peaked between 2 and 3 weeks later. Western blot showed a significant increase of HSP47 and HSP70 7 days after injury. At 2 weeks postinjury, HSP27 expression peaked. Ligth microscopy showed a neointima formation, discontinuity of the media layer and a rich infiltrate. Among infiltrating cells electron microscopy identified dendritic‐like cells in contact with lymphocytes.
Our model of surgical injury induces a significant inflammatory process characterized by enhanced NF‐κB activity and HSPs hyperexpression. Dendritic‐like cells were for the first time identified as a novel component of tissue repair consequent to acute arterial injury.
British Journal of Pharmacology (2006) 147, 175–182. doi:10.1038/sj.bjp.0706472</description><subject>Acute Disease</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Carotid Arteries - metabolism</subject><subject>Carotid Arteries - pathology</subject><subject>Carotid Arteries - ultrastructure</subject><subject>Carotid Artery Injuries - etiology</subject><subject>Carotid Artery Injuries - metabolism</subject><subject>Carotid Artery Injuries - pathology</subject><subject>carotid injury</subject><subject>Endothelium, Vascular - pathology</subject><subject>Endothelium, Vascular - ultrastructure</subject><subject>heat shock protein</subject><subject>Heat-Shock Proteins - biosynthesis</subject><subject>HSP27 Heat-Shock Proteins</subject><subject>HSP47 Heat-Shock Proteins - biosynthesis</subject><subject>HSP70 Heat-Shock Proteins - biosynthesis</subject><subject>Immunohistochemistry</subject><subject>Inflammation - metabolism</subject><subject>Kinetics</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Microscopy, Electron</subject><subject>Neoplasm Proteins - biosynthesis</subject><subject>NF-kappa B - metabolism</subject><subject>Nuclear factor kappa B</subject><subject>Pharmacology. Drug treatments</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>remodeling</subject><subject>Tunica Intima - pathology</subject><subject>Tunica Media - pathology</subject><subject>Vascular Surgical Procedures - adverse effects</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkc2L1DAYxoMo7rh69ShB0FvHpGk-ehF0UXdhQQ96Du-kb2dT2mZM2pH-92ac4qoXTwl5fnnej4eQ55xtORPmTeq2u-6wZZqpSpcPyIZXWhVSGP6QbBhjuuDcmAvyJKWOsSxq-ZhccFXWtazMhuxvxraHYYApxIXiEccpUT9SoEdIbu4h0ohDaLD3457-umS5mR02dLfQNMe9d3B66-ZsMAU63SGNMFEHMUy-oRAnjMtT8qiFPuGz9bwk3z5--Hp1Xdx-_nRz9e62cJWpTQEMFbJGtYbXsBOlAJSq1JIhSs3AyV3LHdYNw0q0bc2w1VyJspGVRKEdikvy9ux7mHcDNi7PE6G3h-gHiIsN4O3fyujv7D4cLVdcGimywevVIIbvM6bJDj457HsYMczJ6rxqYzTP4Mt_wC7McczD2ZJrXivBT27bM-RiSCli-7sTzuwpQJs6mwO0a4D5w4s_-7_H18Qy8GoFcj7QtxFG59M9p1XelqgzJ87cD9_j8p-y9v2X61JKI34Cwv-3OQ</recordid><startdate>200601</startdate><enddate>200601</enddate><creator>Rinaldi, Barbara</creator><creator>Romagnoli, Paolo</creator><creator>Bacci, Stefano</creator><creator>Carnuccio, Rosa</creator><creator>Maiuri, Maria Chiara</creator><creator>Donniacuo, Maria</creator><creator>Capuano, Annalisa</creator><creator>Rossi, Francesco</creator><creator>Filippelli, Amelia</creator><general>Blackwell Publishing Ltd</general><general>Nature Publishing</general><general>Nature Publishing Group</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>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200601</creationdate><title>Inflammatory events in a vascular remodeling model induced by surgical injury to the rat carotid artery</title><author>Rinaldi, Barbara ; Romagnoli, Paolo ; Bacci, Stefano ; Carnuccio, Rosa ; Maiuri, Maria Chiara ; Donniacuo, Maria ; Capuano, Annalisa ; Rossi, Francesco ; Filippelli, Amelia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4898-a0e6e0d6f819ab323ae562750ee570ac5bf1ce9d0e43ff90ef71632d545e37ce3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Acute Disease</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Carotid Arteries - metabolism</topic><topic>Carotid Arteries - pathology</topic><topic>Carotid Arteries - ultrastructure</topic><topic>Carotid Artery Injuries - etiology</topic><topic>Carotid Artery Injuries - metabolism</topic><topic>Carotid Artery Injuries - pathology</topic><topic>carotid injury</topic><topic>Endothelium, Vascular - pathology</topic><topic>Endothelium, Vascular - ultrastructure</topic><topic>heat shock protein</topic><topic>Heat-Shock Proteins - biosynthesis</topic><topic>HSP27 Heat-Shock Proteins</topic><topic>HSP47 Heat-Shock Proteins - biosynthesis</topic><topic>HSP70 Heat-Shock Proteins - biosynthesis</topic><topic>Immunohistochemistry</topic><topic>Inflammation - metabolism</topic><topic>Kinetics</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Microscopy, Electron</topic><topic>Neoplasm Proteins - biosynthesis</topic><topic>NF-kappa B - metabolism</topic><topic>Nuclear factor kappa B</topic><topic>Pharmacology. Drug treatments</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>remodeling</topic><topic>Tunica Intima - pathology</topic><topic>Tunica Media - pathology</topic><topic>Vascular Surgical Procedures - adverse effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rinaldi, Barbara</creatorcontrib><creatorcontrib>Romagnoli, Paolo</creatorcontrib><creatorcontrib>Bacci, Stefano</creatorcontrib><creatorcontrib>Carnuccio, Rosa</creatorcontrib><creatorcontrib>Maiuri, Maria Chiara</creatorcontrib><creatorcontrib>Donniacuo, Maria</creatorcontrib><creatorcontrib>Capuano, Annalisa</creatorcontrib><creatorcontrib>Rossi, Francesco</creatorcontrib><creatorcontrib>Filippelli, Amelia</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>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rinaldi, Barbara</au><au>Romagnoli, Paolo</au><au>Bacci, Stefano</au><au>Carnuccio, Rosa</au><au>Maiuri, Maria Chiara</au><au>Donniacuo, Maria</au><au>Capuano, Annalisa</au><au>Rossi, Francesco</au><au>Filippelli, Amelia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inflammatory events in a vascular remodeling model induced by surgical injury to the rat carotid artery</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>2006-01</date><risdate>2006</risdate><volume>147</volume><issue>2</issue><spage>175</spage><epage>182</epage><pages>175-182</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><coden>BJPCBM</coden><abstract>The aim of our study was to gain insight into the molecular and cellular mechanisms of the inflammatory response to arterial injury in a rat experimental model.
Rats (five for each experimental time) were subjected to brief clamping and longitudinal incision of a carotid artery and monitored for 30 days. Subsequently, Nuclear Factor‐kappaB (NF‐κB) expression was measured by electrophoretic mobility shift assay. Heat shock protein (HSP) 27, HSP47 and HSP70 were evaluated by Western blot. Morphological changes of the vessel wall were investigated by light and electron microscopy.
In injured rat carotid artery NF‐κB activity started immediately upon injury, and peaked between 2 and 3 weeks later. Western blot showed a significant increase of HSP47 and HSP70 7 days after injury. At 2 weeks postinjury, HSP27 expression peaked. Ligth microscopy showed a neointima formation, discontinuity of the media layer and a rich infiltrate. Among infiltrating cells electron microscopy identified dendritic‐like cells in contact with lymphocytes.
Our model of surgical injury induces a significant inflammatory process characterized by enhanced NF‐κB activity and HSPs hyperexpression. Dendritic‐like cells were for the first time identified as a novel component of tissue repair consequent to acute arterial injury.
British Journal of Pharmacology (2006) 147, 175–182. doi:10.1038/sj.bjp.0706472</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>16299548</pmid><doi>10.1038/sj.bjp.0706472</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | British journal of pharmacology, 2006-01, Vol.147 (2), p.175-182 |
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| source | MEDLINE; Access via Wiley Online Library; EZB-FREE-00999 freely available EZB journals; Wiley Online Library (Open Access Collection); PubMed Central; Alma/SFX Local Collection |
| subjects | Acute Disease Animals Biological and medical sciences Carotid Arteries - metabolism Carotid Arteries - pathology Carotid Arteries - ultrastructure Carotid Artery Injuries - etiology Carotid Artery Injuries - metabolism Carotid Artery Injuries - pathology carotid injury Endothelium, Vascular - pathology Endothelium, Vascular - ultrastructure heat shock protein Heat-Shock Proteins - biosynthesis HSP27 Heat-Shock Proteins HSP47 Heat-Shock Proteins - biosynthesis HSP70 Heat-Shock Proteins - biosynthesis Immunohistochemistry Inflammation - metabolism Kinetics Male Medical sciences Microscopy, Electron Neoplasm Proteins - biosynthesis NF-kappa B - metabolism Nuclear factor kappa B Pharmacology. Drug treatments Rats Rats, Wistar remodeling Tunica Intima - pathology Tunica Media - pathology Vascular Surgical Procedures - adverse effects |
| title | Inflammatory events in a vascular remodeling model induced by surgical injury to the rat carotid artery |
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