HIV-1 induces cardiomyopathyby cardiomyocyte invasion and gp120, Tat, and cytokine apoptotic signaling
We examined heart tissues of AIDS patients with or without HIV cardiomyopathy (HIVCM) by immunohistochemistry, in situ polymerase chain reaction, in situ riboprobe hybridization, and the TUNEL technique for apoptosis. In HIVCM tissues, only inflammatory cells, but not endothelial cells or cardiomyoc...
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| Veröffentlicht in: | Cardiovascular toxicology 2004, Vol.4 (2), p.97-108 |
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| creator | Fiala, Milan Popik, Waldemar Qiao, Jian-Hua Lossinsky, Albert S Alce, Timothy Tran, Kenix Yang, Wendy Roos, Kenneth P Arthos, James |
| description | We examined heart tissues of AIDS patients with or without HIV cardiomyopathy (HIVCM) by immunohistochemistry, in situ polymerase chain reaction, in situ riboprobe hybridization, and the TUNEL technique for apoptosis. In HIVCM tissues, only inflammatory cells, but not endothelial cells or cardiomyocytes, displayed HIV-1 DNA and RNA. However, macrophages, lymphocytes, and--in a patchy fashion--cardiomyocytes and endothelial cells exhibited virus envelope protein gp120. Macrophages infiltrated the myocardium in a perivascular fashion and expressed tumor necrosis factor family ligands; adjacent cardiomyocytes suffered apoptosis. In vitro HIV-1 strongly invaded neonatal rat ventricular myocytes (NRVMs) and coronary artery endothelial cells (CAECs) and induced microvilli but did not replicate. HIV-1, gp120, or Tat induced Erk 1/2 phosphorylation, activation of caspase-3, and apoptosis of NRVMs and CAECs; all of these were inhibited by a MAPK/ERK-kinase (MEK) inhibitor U0126. The pathogenesis of HIVCM involves HIV-1 replication in inflammatory cells and induction of cardiomyocyte apoptosis by (1) the extrinsic pathway through apoptotic ligands and (2) the intrinsic pathway through direct virus entry and gp120- and Tat-proapoptotic signaling. |
| doi_str_mv | 10.1385/CT:4:2:097 |
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In HIVCM tissues, only inflammatory cells, but not endothelial cells or cardiomyocytes, displayed HIV-1 DNA and RNA. However, macrophages, lymphocytes, and--in a patchy fashion--cardiomyocytes and endothelial cells exhibited virus envelope protein gp120. Macrophages infiltrated the myocardium in a perivascular fashion and expressed tumor necrosis factor family ligands; adjacent cardiomyocytes suffered apoptosis. In vitro HIV-1 strongly invaded neonatal rat ventricular myocytes (NRVMs) and coronary artery endothelial cells (CAECs) and induced microvilli but did not replicate. HIV-1, gp120, or Tat induced Erk 1/2 phosphorylation, activation of caspase-3, and apoptosis of NRVMs and CAECs; all of these were inhibited by a MAPK/ERK-kinase (MEK) inhibitor U0126. The pathogenesis of HIVCM involves HIV-1 replication in inflammatory cells and induction of cardiomyocyte apoptosis by (1) the extrinsic pathway through apoptotic ligands and (2) the intrinsic pathway through direct virus entry and gp120- and Tat-proapoptotic signaling.</description><identifier>ISSN: 1530-7905</identifier><identifier>EISSN: 1530-7905</identifier><identifier>DOI: 10.1385/CT:4:2:097</identifier><identifier>PMID: 15371627</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Animals, Newborn ; Apoptosis ; Cardiomyopathies - etiology ; Cardiomyopathies - metabolism ; Cardiomyopathies - pathology ; Caspase 3 ; Caspases - metabolism ; Cells, Cultured ; Coronary Vessels - metabolism ; Coronary Vessels - pathology ; Coronary Vessels - ultrastructure ; Cytokines - physiology ; DNA, Viral - metabolism ; Endothelial Cells - metabolism ; Endothelial Cells - pathology ; Endothelial Cells - ultrastructure ; Extracellular Signal-Regulated MAP Kinases - metabolism ; Gene Products, tat - physiology ; HIV Envelope Protein gp120 - physiology ; HIV Infections - complications ; HIV-1 ; Human immunodeficiency virus 1 ; Humans ; Immunohistochemistry ; In Situ Hybridization ; In Situ Nick-End Labeling ; Macrophages - virology ; Myocytes, Cardiac - metabolism ; Myocytes, Cardiac - pathology ; Myocytes, Cardiac - ultrastructure ; Phosphorylation ; Polymerase Chain Reaction ; Rats ; RNA, Viral - metabolism ; Signal Transduction ; tat Gene Products, Human Immunodeficiency Virus</subject><ispartof>Cardiovascular toxicology, 2004, Vol.4 (2), p.97-108</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c1617-be637cfbf16a8fc942cf34c632e1a86bc8c526b2c90c049f2c2eb1759d81e68b3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,4010,27900,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15371627$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fiala, Milan</creatorcontrib><creatorcontrib>Popik, Waldemar</creatorcontrib><creatorcontrib>Qiao, Jian-Hua</creatorcontrib><creatorcontrib>Lossinsky, Albert S</creatorcontrib><creatorcontrib>Alce, Timothy</creatorcontrib><creatorcontrib>Tran, Kenix</creatorcontrib><creatorcontrib>Yang, Wendy</creatorcontrib><creatorcontrib>Roos, Kenneth P</creatorcontrib><creatorcontrib>Arthos, James</creatorcontrib><title>HIV-1 induces cardiomyopathyby cardiomyocyte invasion and gp120, Tat, and cytokine apoptotic signaling</title><title>Cardiovascular toxicology</title><addtitle>Cardiovasc Toxicol</addtitle><description>We examined heart tissues of AIDS patients with or without HIV cardiomyopathy (HIVCM) by immunohistochemistry, in situ polymerase chain reaction, in situ riboprobe hybridization, and the TUNEL technique for apoptosis. In HIVCM tissues, only inflammatory cells, but not endothelial cells or cardiomyocytes, displayed HIV-1 DNA and RNA. However, macrophages, lymphocytes, and--in a patchy fashion--cardiomyocytes and endothelial cells exhibited virus envelope protein gp120. Macrophages infiltrated the myocardium in a perivascular fashion and expressed tumor necrosis factor family ligands; adjacent cardiomyocytes suffered apoptosis. In vitro HIV-1 strongly invaded neonatal rat ventricular myocytes (NRVMs) and coronary artery endothelial cells (CAECs) and induced microvilli but did not replicate. HIV-1, gp120, or Tat induced Erk 1/2 phosphorylation, activation of caspase-3, and apoptosis of NRVMs and CAECs; all of these were inhibited by a MAPK/ERK-kinase (MEK) inhibitor U0126. The pathogenesis of HIVCM involves HIV-1 replication in inflammatory cells and induction of cardiomyocyte apoptosis by (1) the extrinsic pathway through apoptotic ligands and (2) the intrinsic pathway through direct virus entry and gp120- and Tat-proapoptotic signaling.</description><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Apoptosis</subject><subject>Cardiomyopathies - etiology</subject><subject>Cardiomyopathies - metabolism</subject><subject>Cardiomyopathies - pathology</subject><subject>Caspase 3</subject><subject>Caspases - metabolism</subject><subject>Cells, Cultured</subject><subject>Coronary Vessels - metabolism</subject><subject>Coronary Vessels - pathology</subject><subject>Coronary Vessels - ultrastructure</subject><subject>Cytokines - physiology</subject><subject>DNA, Viral - metabolism</subject><subject>Endothelial Cells - metabolism</subject><subject>Endothelial Cells - pathology</subject><subject>Endothelial Cells - ultrastructure</subject><subject>Extracellular Signal-Regulated MAP Kinases - metabolism</subject><subject>Gene Products, tat - physiology</subject><subject>HIV Envelope Protein gp120 - physiology</subject><subject>HIV Infections - complications</subject><subject>HIV-1</subject><subject>Human immunodeficiency virus 1</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>In Situ Hybridization</subject><subject>In Situ Nick-End Labeling</subject><subject>Macrophages - virology</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Myocytes, Cardiac - pathology</subject><subject>Myocytes, Cardiac - ultrastructure</subject><subject>Phosphorylation</subject><subject>Polymerase Chain Reaction</subject><subject>Rats</subject><subject>RNA, Viral - metabolism</subject><subject>Signal Transduction</subject><subject>tat Gene Products, Human Immunodeficiency Virus</subject><issn>1530-7905</issn><issn>1530-7905</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0E1LwzAYB_AgipvTix9AevIgqyZpmqS7SVE3GHipXkOSJjPaNbVphX57qxvMm6fn7cdz-ANwieAtSnh6lxcLssALmLEjMEVpAmOWwfT4Tz8BZyG8Q4gxpukpmIwHhihmU2CXq9cYRa4ue21CpGVbOr8dfCO7t0ENh4UeOjOyLxmcryNZl9GmQRjOo0J28995FP7D1SaSjW863zkdBbepZeXqzTk4sbIK5mJfZ-Dl8aHIl_H6-WmV369jjShisTI0Ydoqi6jkVmcEa5sQTRNskORUaa5TTBXWGdSQZBZrbBRiaVZyZChXyQxc7_42rf_sTejE1gVtqkrWxvdBUMo5pAn5FyLGCSaEjvBmB3XrQ2iNFU3rtrIdBILiJ36RF4IILMb4R3y1_9qrrSkPdJ938g0OuoBU</recordid><startdate>2004</startdate><enddate>2004</enddate><creator>Fiala, Milan</creator><creator>Popik, Waldemar</creator><creator>Qiao, Jian-Hua</creator><creator>Lossinsky, Albert S</creator><creator>Alce, Timothy</creator><creator>Tran, Kenix</creator><creator>Yang, Wendy</creator><creator>Roos, Kenneth P</creator><creator>Arthos, James</creator><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>7U9</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>2004</creationdate><title>HIV-1 induces cardiomyopathyby cardiomyocyte invasion and gp120, Tat, and cytokine apoptotic signaling</title><author>Fiala, Milan ; Popik, Waldemar ; Qiao, Jian-Hua ; Lossinsky, Albert S ; Alce, Timothy ; Tran, Kenix ; Yang, Wendy ; Roos, Kenneth P ; Arthos, James</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c1617-be637cfbf16a8fc942cf34c632e1a86bc8c526b2c90c049f2c2eb1759d81e68b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Apoptosis</topic><topic>Cardiomyopathies - etiology</topic><topic>Cardiomyopathies - metabolism</topic><topic>Cardiomyopathies - pathology</topic><topic>Caspase 3</topic><topic>Caspases - metabolism</topic><topic>Cells, Cultured</topic><topic>Coronary Vessels - metabolism</topic><topic>Coronary Vessels - pathology</topic><topic>Coronary Vessels - ultrastructure</topic><topic>Cytokines - physiology</topic><topic>DNA, Viral - metabolism</topic><topic>Endothelial Cells - metabolism</topic><topic>Endothelial Cells - pathology</topic><topic>Endothelial Cells - ultrastructure</topic><topic>Extracellular Signal-Regulated MAP Kinases - metabolism</topic><topic>Gene Products, tat - physiology</topic><topic>HIV Envelope Protein gp120 - physiology</topic><topic>HIV Infections - complications</topic><topic>HIV-1</topic><topic>Human immunodeficiency virus 1</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>In Situ Hybridization</topic><topic>In Situ Nick-End Labeling</topic><topic>Macrophages - virology</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Myocytes, Cardiac - pathology</topic><topic>Myocytes, Cardiac - ultrastructure</topic><topic>Phosphorylation</topic><topic>Polymerase Chain Reaction</topic><topic>Rats</topic><topic>RNA, Viral - metabolism</topic><topic>Signal Transduction</topic><topic>tat Gene Products, Human Immunodeficiency Virus</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fiala, Milan</creatorcontrib><creatorcontrib>Popik, Waldemar</creatorcontrib><creatorcontrib>Qiao, Jian-Hua</creatorcontrib><creatorcontrib>Lossinsky, Albert S</creatorcontrib><creatorcontrib>Alce, Timothy</creatorcontrib><creatorcontrib>Tran, Kenix</creatorcontrib><creatorcontrib>Yang, Wendy</creatorcontrib><creatorcontrib>Roos, Kenneth P</creatorcontrib><creatorcontrib>Arthos, James</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cardiovascular toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fiala, Milan</au><au>Popik, Waldemar</au><au>Qiao, Jian-Hua</au><au>Lossinsky, Albert S</au><au>Alce, Timothy</au><au>Tran, Kenix</au><au>Yang, Wendy</au><au>Roos, Kenneth P</au><au>Arthos, James</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>HIV-1 induces cardiomyopathyby cardiomyocyte invasion and gp120, Tat, and cytokine apoptotic signaling</atitle><jtitle>Cardiovascular toxicology</jtitle><addtitle>Cardiovasc Toxicol</addtitle><date>2004</date><risdate>2004</risdate><volume>4</volume><issue>2</issue><spage>97</spage><epage>108</epage><pages>97-108</pages><issn>1530-7905</issn><eissn>1530-7905</eissn><abstract>We examined heart tissues of AIDS patients with or without HIV cardiomyopathy (HIVCM) by immunohistochemistry, in situ polymerase chain reaction, in situ riboprobe hybridization, and the TUNEL technique for apoptosis. In HIVCM tissues, only inflammatory cells, but not endothelial cells or cardiomyocytes, displayed HIV-1 DNA and RNA. However, macrophages, lymphocytes, and--in a patchy fashion--cardiomyocytes and endothelial cells exhibited virus envelope protein gp120. Macrophages infiltrated the myocardium in a perivascular fashion and expressed tumor necrosis factor family ligands; adjacent cardiomyocytes suffered apoptosis. In vitro HIV-1 strongly invaded neonatal rat ventricular myocytes (NRVMs) and coronary artery endothelial cells (CAECs) and induced microvilli but did not replicate. HIV-1, gp120, or Tat induced Erk 1/2 phosphorylation, activation of caspase-3, and apoptosis of NRVMs and CAECs; all of these were inhibited by a MAPK/ERK-kinase (MEK) inhibitor U0126. 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| subjects | Animals Animals, Newborn Apoptosis Cardiomyopathies - etiology Cardiomyopathies - metabolism Cardiomyopathies - pathology Caspase 3 Caspases - metabolism Cells, Cultured Coronary Vessels - metabolism Coronary Vessels - pathology Coronary Vessels - ultrastructure Cytokines - physiology DNA, Viral - metabolism Endothelial Cells - metabolism Endothelial Cells - pathology Endothelial Cells - ultrastructure Extracellular Signal-Regulated MAP Kinases - metabolism Gene Products, tat - physiology HIV Envelope Protein gp120 - physiology HIV Infections - complications HIV-1 Human immunodeficiency virus 1 Humans Immunohistochemistry In Situ Hybridization In Situ Nick-End Labeling Macrophages - virology Myocytes, Cardiac - metabolism Myocytes, Cardiac - pathology Myocytes, Cardiac - ultrastructure Phosphorylation Polymerase Chain Reaction Rats RNA, Viral - metabolism Signal Transduction tat Gene Products, Human Immunodeficiency Virus |
| title | HIV-1 induces cardiomyopathyby cardiomyocyte invasion and gp120, Tat, and cytokine apoptotic signaling |
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