Mediators of perivascular inflammation in the left ventricle of renovascular hypertensive rats
Inflammatory cells invade the fibrotic myocardium of spontaneously hypertensive rats at the same sites as where fibroblasts are produced. The role of these inflammatory cells in myocardial fibrogenesis was studied in the present work. The production and distribution of proteins that may be implicate...
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| Veröffentlicht in: | Cardiovascular research 1996-04, Vol.31 (4), p.585-595 |
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| description | Inflammatory cells invade the fibrotic myocardium of spontaneously hypertensive rats at the same sites as where fibroblasts are produced. The role of these inflammatory cells in myocardial fibrogenesis was studied in the present work.
The production and distribution of proteins that may be implicated in inflammation was examined by immunohistochemistry of sections of left ventricles from 1-month and 4-month renovascular hypertensive and age-matched control rats using antibodies against ICAM-1, LFA-1, TGF beta 1, PDGF-A, T and H kininogens, IgG, IgM, C3, and C5b-9. Infiltrating inflammatory cells were phenotyped by immunohistochemistry. The TGF beta 1 and PDGF-A mRNA levels were checked by RT-PCR.
Infiltrating cells were mainly T helper lymphocytes and macrophages, and there were more inflammatory cells in hypertensive rats than in control rats, localized especially around coronary arteries and in microscars. There were more ICAM-1 and LFA-1 in the ventricles of hypertensive than in control rats at 1 month, but the ICAM-1 expressions in hypertensive and control rats were similar at 4 months. TGF beta 1 and PDGF-A mRNA steady states increased in 4-month hypertensive rats, but there was no labeling for TGF beta or PDGF by immunohistochemistry. There was only faint labeling for T and H kininogens, and it was not increased in hypertensive rats. There were deposits of IgM and C5b-9 only in hypertensive rats.
Thus, inflammatory cells infiltrate the cardiac tissue of renovascular hypertensive rats as in the case of spontaneously hypertensive rats and these cells may use the ICAM-1/LFA-1 system to infiltrate, but neither TGF beta 1 and PDGF-A, nor the kininogen system seem to be associated with cardiac fibrogenesis. Otherwise, the complement system could act as arteriosclerotic and/or leukocyte mobilizing factors. |
| doi_str_mv | 10.1016/0008-6363(95)00239-1 |
| format | Article |
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The production and distribution of proteins that may be implicated in inflammation was examined by immunohistochemistry of sections of left ventricles from 1-month and 4-month renovascular hypertensive and age-matched control rats using antibodies against ICAM-1, LFA-1, TGF beta 1, PDGF-A, T and H kininogens, IgG, IgM, C3, and C5b-9. Infiltrating inflammatory cells were phenotyped by immunohistochemistry. The TGF beta 1 and PDGF-A mRNA levels were checked by RT-PCR.
Infiltrating cells were mainly T helper lymphocytes and macrophages, and there were more inflammatory cells in hypertensive rats than in control rats, localized especially around coronary arteries and in microscars. There were more ICAM-1 and LFA-1 in the ventricles of hypertensive than in control rats at 1 month, but the ICAM-1 expressions in hypertensive and control rats were similar at 4 months. TGF beta 1 and PDGF-A mRNA steady states increased in 4-month hypertensive rats, but there was no labeling for TGF beta or PDGF by immunohistochemistry. There was only faint labeling for T and H kininogens, and it was not increased in hypertensive rats. There were deposits of IgM and C5b-9 only in hypertensive rats.
Thus, inflammatory cells infiltrate the cardiac tissue of renovascular hypertensive rats as in the case of spontaneously hypertensive rats and these cells may use the ICAM-1/LFA-1 system to infiltrate, but neither TGF beta 1 and PDGF-A, nor the kininogen system seem to be associated with cardiac fibrogenesis. Otherwise, the complement system could act as arteriosclerotic and/or leukocyte mobilizing factors.</description><identifier>ISSN: 0008-6363</identifier><identifier>EISSN: 1755-3245</identifier><identifier>DOI: 10.1016/0008-6363(95)00239-1</identifier><identifier>PMID: 8689650</identifier><identifier>CODEN: CVREAU</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Animals ; Arterial hypertension. Arterial hypotension ; Base Sequence ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Cell Adhesion Molecules - metabolism ; Complement C3 - metabolism ; Complement Membrane Attack Complex - metabolism ; DNA Primers - genetics ; E-Selectin - metabolism ; Experimental diseases ; Fibrosis ; Hypertension, Renovascular - immunology ; Hypertension, Renovascular - metabolism ; Hypertension, Renovascular - pathology ; Immunoglobulin M - metabolism ; Immunohistochemistry ; Intercellular Adhesion Molecule-1 - metabolism ; Kininogens - metabolism ; Lymphocyte Function-Associated Antigen-1 - metabolism ; Macrophages - pathology ; Medical sciences ; Molecular Sequence Data ; Myocardium - immunology ; Myocardium - metabolism ; Myocardium - pathology ; Platelet-Derived Growth Factor - genetics ; Platelet-Derived Growth Factor - metabolism ; Polymerase Chain Reaction ; Rats ; Rats, Wistar ; T-Lymphocytes, Helper-Inducer - pathology ; Transforming Growth Factor beta - genetics ; Transforming Growth Factor beta - metabolism</subject><ispartof>Cardiovascular research, 1996-04, Vol.31 (4), p.585-595</ispartof><rights>1996 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c331t-c178781835cfc06af05776f7f0415c2bb0406c0deea4aa9732ffe51dcffb993f3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3073107$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8689650$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>NICOLETTI, A</creatorcontrib><creatorcontrib>MANDET, C</creatorcontrib><creatorcontrib>CHALLAH, M</creatorcontrib><creatorcontrib>BARIETY, J</creatorcontrib><creatorcontrib>MICHEL, J.-B</creatorcontrib><title>Mediators of perivascular inflammation in the left ventricle of renovascular hypertensive rats</title><title>Cardiovascular research</title><addtitle>Cardiovasc Res</addtitle><description>Inflammatory cells invade the fibrotic myocardium of spontaneously hypertensive rats at the same sites as where fibroblasts are produced. The role of these inflammatory cells in myocardial fibrogenesis was studied in the present work.
The production and distribution of proteins that may be implicated in inflammation was examined by immunohistochemistry of sections of left ventricles from 1-month and 4-month renovascular hypertensive and age-matched control rats using antibodies against ICAM-1, LFA-1, TGF beta 1, PDGF-A, T and H kininogens, IgG, IgM, C3, and C5b-9. Infiltrating inflammatory cells were phenotyped by immunohistochemistry. The TGF beta 1 and PDGF-A mRNA levels were checked by RT-PCR.
Infiltrating cells were mainly T helper lymphocytes and macrophages, and there were more inflammatory cells in hypertensive rats than in control rats, localized especially around coronary arteries and in microscars. There were more ICAM-1 and LFA-1 in the ventricles of hypertensive than in control rats at 1 month, but the ICAM-1 expressions in hypertensive and control rats were similar at 4 months. TGF beta 1 and PDGF-A mRNA steady states increased in 4-month hypertensive rats, but there was no labeling for TGF beta or PDGF by immunohistochemistry. There was only faint labeling for T and H kininogens, and it was not increased in hypertensive rats. There were deposits of IgM and C5b-9 only in hypertensive rats.
Thus, inflammatory cells infiltrate the cardiac tissue of renovascular hypertensive rats as in the case of spontaneously hypertensive rats and these cells may use the ICAM-1/LFA-1 system to infiltrate, but neither TGF beta 1 and PDGF-A, nor the kininogen system seem to be associated with cardiac fibrogenesis. Otherwise, the complement system could act as arteriosclerotic and/or leukocyte mobilizing factors.</description><subject>Animals</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Base Sequence</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Cell Adhesion Molecules - metabolism</subject><subject>Complement C3 - metabolism</subject><subject>Complement Membrane Attack Complex - metabolism</subject><subject>DNA Primers - genetics</subject><subject>E-Selectin - metabolism</subject><subject>Experimental diseases</subject><subject>Fibrosis</subject><subject>Hypertension, Renovascular - immunology</subject><subject>Hypertension, Renovascular - metabolism</subject><subject>Hypertension, Renovascular - pathology</subject><subject>Immunoglobulin M - metabolism</subject><subject>Immunohistochemistry</subject><subject>Intercellular Adhesion Molecule-1 - metabolism</subject><subject>Kininogens - metabolism</subject><subject>Lymphocyte Function-Associated Antigen-1 - metabolism</subject><subject>Macrophages - pathology</subject><subject>Medical sciences</subject><subject>Molecular Sequence Data</subject><subject>Myocardium - immunology</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>Platelet-Derived Growth Factor - genetics</subject><subject>Platelet-Derived Growth Factor - metabolism</subject><subject>Polymerase Chain Reaction</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>T-Lymphocytes, Helper-Inducer - pathology</subject><subject>Transforming Growth Factor beta - genetics</subject><subject>Transforming Growth Factor beta - metabolism</subject><issn>0008-6363</issn><issn>1755-3245</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kMtKAzEUhoMotVbfQGEWIroYPWkmk5mlFG9QcaNbQyZzQiNzqUmm0Lc3Y0sXh8PPf1l8hFxSuKdA8wcAKNKc5ey25HcAc1am9IhMqeA8ZfOMH5PpIXJKzrz_iZJzkU3IpMiLMucwJd_vWFsVeueT3iRrdHajvB4a5RLbmUa1rQq276JIwgqTBk1INtgFZ3WDY8Vh1x8qq21cCNh5u8HEqeDPyYlRjceL_Z-Rr-enz8Vruvx4eVs8LlPNGA2ppqIQBS0Y10ZDrgxwIXIjDGSU63lVQQa5hhpRZUqVgs2NQU5rbUxVlsywGbnZ7a5d_zugD7K1XmPTqA77wcs4LkCULAazXVC73nuHRq6dbZXbSgpyxCpHZnJkJksu_7FKGmtX-_2harE-lPYco3-99yMK1RinOm39IcZAMBrvD_f-gbc</recordid><startdate>19960401</startdate><enddate>19960401</enddate><creator>NICOLETTI, A</creator><creator>MANDET, C</creator><creator>CHALLAH, M</creator><creator>BARIETY, J</creator><creator>MICHEL, J.-B</creator><general>Oxford University Press</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>19960401</creationdate><title>Mediators of perivascular inflammation in the left ventricle of renovascular hypertensive rats</title><author>NICOLETTI, A ; MANDET, C ; CHALLAH, M ; BARIETY, J ; MICHEL, J.-B</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c331t-c178781835cfc06af05776f7f0415c2bb0406c0deea4aa9732ffe51dcffb993f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Animals</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Base Sequence</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Cell Adhesion Molecules - metabolism</topic><topic>Complement C3 - metabolism</topic><topic>Complement Membrane Attack Complex - metabolism</topic><topic>DNA Primers - genetics</topic><topic>E-Selectin - metabolism</topic><topic>Experimental diseases</topic><topic>Fibrosis</topic><topic>Hypertension, Renovascular - immunology</topic><topic>Hypertension, Renovascular - metabolism</topic><topic>Hypertension, Renovascular - pathology</topic><topic>Immunoglobulin M - metabolism</topic><topic>Immunohistochemistry</topic><topic>Intercellular Adhesion Molecule-1 - metabolism</topic><topic>Kininogens - metabolism</topic><topic>Lymphocyte Function-Associated Antigen-1 - metabolism</topic><topic>Macrophages - pathology</topic><topic>Medical sciences</topic><topic>Molecular Sequence Data</topic><topic>Myocardium - immunology</topic><topic>Myocardium - metabolism</topic><topic>Myocardium - pathology</topic><topic>Platelet-Derived Growth Factor - genetics</topic><topic>Platelet-Derived Growth Factor - metabolism</topic><topic>Polymerase Chain Reaction</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>T-Lymphocytes, Helper-Inducer - pathology</topic><topic>Transforming Growth Factor beta - genetics</topic><topic>Transforming Growth Factor beta - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>NICOLETTI, A</creatorcontrib><creatorcontrib>MANDET, C</creatorcontrib><creatorcontrib>CHALLAH, M</creatorcontrib><creatorcontrib>BARIETY, J</creatorcontrib><creatorcontrib>MICHEL, J.-B</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>Cardiovascular research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>NICOLETTI, A</au><au>MANDET, C</au><au>CHALLAH, M</au><au>BARIETY, J</au><au>MICHEL, J.-B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mediators of perivascular inflammation in the left ventricle of renovascular hypertensive rats</atitle><jtitle>Cardiovascular research</jtitle><addtitle>Cardiovasc Res</addtitle><date>1996-04-01</date><risdate>1996</risdate><volume>31</volume><issue>4</issue><spage>585</spage><epage>595</epage><pages>585-595</pages><issn>0008-6363</issn><eissn>1755-3245</eissn><coden>CVREAU</coden><abstract>Inflammatory cells invade the fibrotic myocardium of spontaneously hypertensive rats at the same sites as where fibroblasts are produced. The role of these inflammatory cells in myocardial fibrogenesis was studied in the present work.
The production and distribution of proteins that may be implicated in inflammation was examined by immunohistochemistry of sections of left ventricles from 1-month and 4-month renovascular hypertensive and age-matched control rats using antibodies against ICAM-1, LFA-1, TGF beta 1, PDGF-A, T and H kininogens, IgG, IgM, C3, and C5b-9. Infiltrating inflammatory cells were phenotyped by immunohistochemistry. The TGF beta 1 and PDGF-A mRNA levels were checked by RT-PCR.
Infiltrating cells were mainly T helper lymphocytes and macrophages, and there were more inflammatory cells in hypertensive rats than in control rats, localized especially around coronary arteries and in microscars. There were more ICAM-1 and LFA-1 in the ventricles of hypertensive than in control rats at 1 month, but the ICAM-1 expressions in hypertensive and control rats were similar at 4 months. TGF beta 1 and PDGF-A mRNA steady states increased in 4-month hypertensive rats, but there was no labeling for TGF beta or PDGF by immunohistochemistry. There was only faint labeling for T and H kininogens, and it was not increased in hypertensive rats. There were deposits of IgM and C5b-9 only in hypertensive rats.
Thus, inflammatory cells infiltrate the cardiac tissue of renovascular hypertensive rats as in the case of spontaneously hypertensive rats and these cells may use the ICAM-1/LFA-1 system to infiltrate, but neither TGF beta 1 and PDGF-A, nor the kininogen system seem to be associated with cardiac fibrogenesis. Otherwise, the complement system could act as arteriosclerotic and/or leukocyte mobilizing factors.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>8689650</pmid><doi>10.1016/0008-6363(95)00239-1</doi><tpages>11</tpages></addata></record> |
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| ispartof | Cardiovascular research, 1996-04, Vol.31 (4), p.585-595 |
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| subjects | Animals Arterial hypertension. Arterial hypotension Base Sequence Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Cell Adhesion Molecules - metabolism Complement C3 - metabolism Complement Membrane Attack Complex - metabolism DNA Primers - genetics E-Selectin - metabolism Experimental diseases Fibrosis Hypertension, Renovascular - immunology Hypertension, Renovascular - metabolism Hypertension, Renovascular - pathology Immunoglobulin M - metabolism Immunohistochemistry Intercellular Adhesion Molecule-1 - metabolism Kininogens - metabolism Lymphocyte Function-Associated Antigen-1 - metabolism Macrophages - pathology Medical sciences Molecular Sequence Data Myocardium - immunology Myocardium - metabolism Myocardium - pathology Platelet-Derived Growth Factor - genetics Platelet-Derived Growth Factor - metabolism Polymerase Chain Reaction Rats Rats, Wistar T-Lymphocytes, Helper-Inducer - pathology Transforming Growth Factor beta - genetics Transforming Growth Factor beta - metabolism |
| title | Mediators of perivascular inflammation in the left ventricle of renovascular hypertensive rats |
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