Human Heart Generates Complement Proteins That Are Upregulated and Activated After Myocardial Infarction
In human heart, we detected mRNAs and proteins for C1q, C1r, C1s, C2, C3, C4, C5, C6, C7, C8, and C9 with the use of reverse transcriptase-polymerase chain reaction, Western blotting, and immunohistochemical techniques. We found an upregulation of both mRNAs and proteins in areas of recent and old m...
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| Veröffentlicht in: | Circulation research 1998-10, Vol.83 (8), p.860-869 |
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| creator | Yasojima, Koji Schwab, Claudia McGeer, Edith G McGeer, Patrick L |
| description | In human heart, we detected mRNAs and proteins for C1q, C1r, C1s, C2, C3, C4, C5, C6, C7, C8, and C9 with the use of reverse transcriptase-polymerase chain reaction, Western blotting, and immunohistochemical techniques. We found an upregulation of both mRNAs and proteins in areas of recent and old myocardial infarctions. In both situations, the classical complement pathway was activated, with C4d, C3d, and the membrane attack complex (C5b-9) being deposited on damaged cardiac myocytes. These activated complement components were also identified on Western blots of infarcted tissue. Complement mRNAs in infarcted heart tissue were higher than those in liver, and liver complement mRNAs were not upregulated in cases with infarcted hearts. Our results establish that (1) complement proteins are endogenously produced by human heart; (2) the classical complement pathway is fully activated after myocardial infarction; (3) complement activation is directly involved in myocardial damage after ischemic insults; and (4) damage from complement activation may be chronically sustained. These data suggest that inhibition of the complement system should be effective in treating myocardial infarction. (Circ Res. 1998;83:860-869.) |
| doi_str_mv | 10.1161/01.RES.83.8.860 |
| format | Article |
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We found an upregulation of both mRNAs and proteins in areas of recent and old myocardial infarctions. In both situations, the classical complement pathway was activated, with C4d, C3d, and the membrane attack complex (C5b-9) being deposited on damaged cardiac myocytes. These activated complement components were also identified on Western blots of infarcted tissue. Complement mRNAs in infarcted heart tissue were higher than those in liver, and liver complement mRNAs were not upregulated in cases with infarcted hearts. Our results establish that (1) complement proteins are endogenously produced by human heart; (2) the classical complement pathway is fully activated after myocardial infarction; (3) complement activation is directly involved in myocardial damage after ischemic insults; and (4) damage from complement activation may be chronically sustained. These data suggest that inhibition of the complement system should be effective in treating myocardial infarction. 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Vascular system ; Complement System Proteins - analysis ; Complement System Proteins - genetics ; Complement System Proteins - metabolism ; Coronary heart disease ; DNA Primers ; Female ; Gene Expression ; Heart ; Humans ; Immunohistochemistry ; Male ; Medical sciences ; Middle Aged ; Myocardial Infarction - metabolism ; Myocardium - chemistry ; Myocardium - metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - metabolism</subject><ispartof>Circulation research, 1998-10, Vol.83 (8), p.860-869</ispartof><rights>1998 American Heart Association, Inc.</rights><rights>1998 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Oct 19, 1998</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4700-dfa884a6fc4fbc1887576756831cb37824ac879fa75c95b46c5a9a9649f7377e3</citedby><cites>FETCH-LOGICAL-c4700-dfa884a6fc4fbc1887576756831cb37824ac879fa75c95b46c5a9a9649f7377e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3687,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2432638$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9776733$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yasojima, Koji</creatorcontrib><creatorcontrib>Schwab, Claudia</creatorcontrib><creatorcontrib>McGeer, Edith G</creatorcontrib><creatorcontrib>McGeer, Patrick L</creatorcontrib><title>Human Heart Generates Complement Proteins That Are Upregulated and Activated After Myocardial Infarction</title><title>Circulation research</title><addtitle>Circ Res</addtitle><description>In human heart, we detected mRNAs and proteins for C1q, C1r, C1s, C2, C3, C4, C5, C6, C7, C8, and C9 with the use of reverse transcriptase-polymerase chain reaction, Western blotting, and immunohistochemical techniques. We found an upregulation of both mRNAs and proteins in areas of recent and old myocardial infarctions. In both situations, the classical complement pathway was activated, with C4d, C3d, and the membrane attack complex (C5b-9) being deposited on damaged cardiac myocytes. These activated complement components were also identified on Western blots of infarcted tissue. Complement mRNAs in infarcted heart tissue were higher than those in liver, and liver complement mRNAs were not upregulated in cases with infarcted hearts. Our results establish that (1) complement proteins are endogenously produced by human heart; (2) the classical complement pathway is fully activated after myocardial infarction; (3) complement activation is directly involved in myocardial damage after ischemic insults; and (4) damage from complement activation may be chronically sustained. These data suggest that inhibition of the complement system should be effective in treating myocardial infarction. (Circ Res. 1998;83:860-869.)</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Cardiology. Vascular system</subject><subject>Complement System Proteins - analysis</subject><subject>Complement System Proteins - genetics</subject><subject>Complement System Proteins - metabolism</subject><subject>Coronary heart disease</subject><subject>DNA Primers</subject><subject>Female</subject><subject>Gene Expression</subject><subject>Heart</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Myocardial Infarction - metabolism</subject><subject>Myocardium - chemistry</subject><subject>Myocardium - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - metabolism</subject><issn>0009-7330</issn><issn>1524-4571</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkUFv1DAQRi0EKkvhzAnJQohb0nFsx_ZxtSrdSkUgaM_WrOOwKY6z2AlV_z2GXfXAyZr5nkejeYS8ZVAz1rILYPW3y--15rWudQvPyIrJRlRCKvacrADAVIpzeEle5XwPwARvzBk5M0q1pb8i--0yYqRbj2mmVz76hLPPdDONh-BHH2f6NU2zH2Kmt3uc6Tp5endI_scSCthRjB1du3n4_a9a97NP9PPj5DB1AwZ6HXtMJZ7ia_Kix5D9m9N7Tu4-Xd5uttXNl6vrzfqmckIBVF2PWgtseyf6nWNaK1k2la3mzO240o1Ap5XpUUln5E60TqJB0wrTK66U5-fk43HuIU2_Fp9nOw7Z-RAw-mnJtjVGgQRewPf_gffTkmLZzTasEYwrKQt0cYRcmnJOvreHNIyYHi0D-1eABWaLAKu51bYIKD_encYuu9F3T_zp4iX_cMoxOwx9wuiG_IQ1RVDLdcHEEXuYQrlp_hmWB5_s3mOY97Z4BQ6sqZgxmgEzUJUOA_4HpIicmQ</recordid><startdate>19981019</startdate><enddate>19981019</enddate><creator>Yasojima, Koji</creator><creator>Schwab, Claudia</creator><creator>McGeer, Edith G</creator><creator>McGeer, Patrick L</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>19981019</creationdate><title>Human Heart Generates Complement Proteins That Are Upregulated and Activated After Myocardial Infarction</title><author>Yasojima, Koji ; Schwab, Claudia ; McGeer, Edith G ; McGeer, Patrick L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4700-dfa884a6fc4fbc1887576756831cb37824ac879fa75c95b46c5a9a9649f7377e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Cardiology. Vascular system</topic><topic>Complement System Proteins - analysis</topic><topic>Complement System Proteins - genetics</topic><topic>Complement System Proteins - metabolism</topic><topic>Coronary heart disease</topic><topic>DNA Primers</topic><topic>Female</topic><topic>Gene Expression</topic><topic>Heart</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Myocardial Infarction - metabolism</topic><topic>Myocardium - chemistry</topic><topic>Myocardium - metabolism</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yasojima, Koji</creatorcontrib><creatorcontrib>Schwab, Claudia</creatorcontrib><creatorcontrib>McGeer, Edith G</creatorcontrib><creatorcontrib>McGeer, Patrick L</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>Yasojima, Koji</au><au>Schwab, Claudia</au><au>McGeer, Edith G</au><au>McGeer, Patrick L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Human Heart Generates Complement Proteins That Are Upregulated and Activated After Myocardial Infarction</atitle><jtitle>Circulation research</jtitle><addtitle>Circ Res</addtitle><date>1998-10-19</date><risdate>1998</risdate><volume>83</volume><issue>8</issue><spage>860</spage><epage>869</epage><pages>860-869</pages><issn>0009-7330</issn><eissn>1524-4571</eissn><coden>CIRUAL</coden><abstract>In human heart, we detected mRNAs and proteins for C1q, C1r, C1s, C2, C3, C4, C5, C6, C7, C8, and C9 with the use of reverse transcriptase-polymerase chain reaction, Western blotting, and immunohistochemical techniques. We found an upregulation of both mRNAs and proteins in areas of recent and old myocardial infarctions. In both situations, the classical complement pathway was activated, with C4d, C3d, and the membrane attack complex (C5b-9) being deposited on damaged cardiac myocytes. These activated complement components were also identified on Western blots of infarcted tissue. Complement mRNAs in infarcted heart tissue were higher than those in liver, and liver complement mRNAs were not upregulated in cases with infarcted hearts. Our results establish that (1) complement proteins are endogenously produced by human heart; (2) the classical complement pathway is fully activated after myocardial infarction; (3) complement activation is directly involved in myocardial damage after ischemic insults; and (4) damage from complement activation may be chronically sustained. These data suggest that inhibition of the complement system should be effective in treating myocardial infarction. (Circ Res. 1998;83:860-869.)</abstract><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>9776733</pmid><doi>10.1161/01.RES.83.8.860</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Circulation research, 1998-10, Vol.83 (8), p.860-869 |
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| source | MEDLINE; American Heart Association Journals; Journals@Ovid Complete; EZB-FREE-00999 freely available EZB journals |
| subjects | Adult Aged Aged, 80 and over Biological and medical sciences Blotting, Western Cardiology. Vascular system Complement System Proteins - analysis Complement System Proteins - genetics Complement System Proteins - metabolism Coronary heart disease DNA Primers Female Gene Expression Heart Humans Immunohistochemistry Male Medical sciences Middle Aged Myocardial Infarction - metabolism Myocardium - chemistry Myocardium - metabolism Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - metabolism |
| title | Human Heart Generates Complement Proteins That Are Upregulated and Activated After Myocardial Infarction |
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