Suppressive effects of anti-inflammatory agents on human endothelial cell activation and induction of heat shock proteins.
Identifieur interne : 000A32 ( PubMed/Corpus ); précédent : 000A31; suivant : 000A33Suppressive effects of anti-inflammatory agents on human endothelial cell activation and induction of heat shock proteins.
Auteurs : A. Amberger ; M. Hala ; M. Saurwein-Teissl ; B. Metzler ; B. Grubeck-Loebenstein ; Q. Xu ; G. WickSource :
- Molecular medicine (Cambridge, Mass.) [ 1076-1551 ] ; 1999.
English descriptors
- KwdEn :
- Adult, Anti-Inflammatory Agents, Non-Steroidal (pharmacology), Aspirin (pharmacology), Cell Division (drug effects), Cells, Cultured (drug effects), Cells, Cultured (metabolism), Chaperonin 60 (drug effects), Chaperonin 60 (metabolism), Chemokine CCL2 (metabolism), Cyclosporine (pharmacology), E-Selectin (drug effects), E-Selectin (metabolism), Endothelium, Vascular (cytology), Endothelium, Vascular (drug effects), Endothelium, Vascular (metabolism), Female, HSP70 Heat-Shock Proteins (drug effects), HSP70 Heat-Shock Proteins (metabolism), Heat-Shock Proteins (drug effects), Heat-Shock Proteins (metabolism), Humans, Immunosuppressive Agents (pharmacology), Indomethacin (pharmacology), Intercellular Adhesion Molecule-1 (drug effects), Intercellular Adhesion Molecule-1 (metabolism), Lymphocytes (drug effects), Lymphocytes (metabolism), Male, NF-kappa B (drug effects), NF-kappa B (genetics), NF-kappa B (metabolism), Transcription Factors (drug effects), Transcription Factors (genetics), Transcription Factors (metabolism), Vascular Cell Adhesion Molecule-1 (drug effects), Vascular Cell Adhesion Molecule-1 (metabolism).
- MESH :
- chemical , drug effects : Chaperonin 60, E-Selectin, HSP70 Heat-Shock Proteins, Heat-Shock Proteins, Intercellular Adhesion Molecule-1, NF-kappa B, Transcription Factors, Vascular Cell Adhesion Molecule-1.
- chemical , genetics : NF-kappa B, Transcription Factors.
- chemical , metabolism : Chaperonin 60, Chemokine CCL2, E-Selectin, HSP70 Heat-Shock Proteins, Heat-Shock Proteins, Intercellular Adhesion Molecule-1, NF-kappa B, Transcription Factors, Vascular Cell Adhesion Molecule-1.
- chemical , pharmacology : Anti-Inflammatory Agents, Non-Steroidal, Aspirin, Cyclosporine, Immunosuppressive Agents, Indomethacin.
- cytology : Endothelium, Vascular.
- drug effects : Cell Division, Cells, Cultured, Endothelium, Vascular, Lymphocytes.
- metabolism : Cells, Cultured, Endothelium, Vascular, Lymphocytes.
- Adult, Female, Humans, Male.
Abstract
Studies from our laboratory have shown that the earliest stages of atherosclerosis may be mediated by an autoimmune reaction against heat shock protein 60 (Hsp60). The interactions of Hsp60-specific T cells with arterial endothelial cells (EC) require expression of both Hsp60 and certain adhesion molecules shown to be induced simultaneously in EC by mechanical and other types of stress. Recently, it was shown that suppression of T cell-mediated immune responses by cyclosporin A (CyA) enhanced atherosclerotic lesion formation in mice. In contrast, aspirin was found to lower the risk of myocardial infarction in men. These conflicting observations may be due to different effects of anti-inflammatory agents on adhesion molecule and Hsp expression in EC, respectively.
PubMed: 10203577
Links to Exploration step
pubmed:10203577Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Suppressive effects of anti-inflammatory agents on human endothelial cell activation and induction of heat shock proteins.</title><author><name sortKey="Amberger, A" sort="Amberger, A" uniqKey="Amberger A" first="A" last="Amberger">A. Amberger</name><affiliation><nlm:affiliation>Institute for Biomedical Aging Research, Austrian Academy of Sciences, Innsbruck, Austria.</nlm:affiliation></affiliation></author><author><name sortKey="Hala, M" sort="Hala, M" uniqKey="Hala M" first="M" last="Hala">M. Hala</name></author><author><name sortKey="Saurwein Teissl, M" sort="Saurwein Teissl, M" uniqKey="Saurwein Teissl M" first="M" last="Saurwein-Teissl">M. Saurwein-Teissl</name></author><author><name sortKey="Metzler, B" sort="Metzler, B" uniqKey="Metzler B" first="B" last="Metzler">B. Metzler</name></author><author><name sortKey="Grubeck Loebenstein, B" sort="Grubeck Loebenstein, B" uniqKey="Grubeck Loebenstein B" first="B" last="Grubeck-Loebenstein">B. Grubeck-Loebenstein</name></author><author><name sortKey="Xu, Q" sort="Xu, Q" uniqKey="Xu Q" first="Q" last="Xu">Q. Xu</name></author><author><name sortKey="Wick, G" sort="Wick, G" uniqKey="Wick G" first="G" last="Wick">G. Wick</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1999">1999</date><idno type="RBID">pubmed:10203577</idno><idno type="pmid">10203577</idno><idno type="wicri:Area/PubMed/Corpus">000A32</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000A32</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Suppressive effects of anti-inflammatory agents on human endothelial cell activation and induction of heat shock proteins.</title><author><name sortKey="Amberger, A" sort="Amberger, A" uniqKey="Amberger A" first="A" last="Amberger">A. Amberger</name><affiliation><nlm:affiliation>Institute for Biomedical Aging Research, Austrian Academy of Sciences, Innsbruck, Austria.</nlm:affiliation></affiliation></author><author><name sortKey="Hala, M" sort="Hala, M" uniqKey="Hala M" first="M" last="Hala">M. Hala</name></author><author><name sortKey="Saurwein Teissl, M" sort="Saurwein Teissl, M" uniqKey="Saurwein Teissl M" first="M" last="Saurwein-Teissl">M. Saurwein-Teissl</name></author><author><name sortKey="Metzler, B" sort="Metzler, B" uniqKey="Metzler B" first="B" last="Metzler">B. Metzler</name></author><author><name sortKey="Grubeck Loebenstein, B" sort="Grubeck Loebenstein, B" uniqKey="Grubeck Loebenstein B" first="B" last="Grubeck-Loebenstein">B. Grubeck-Loebenstein</name></author><author><name sortKey="Xu, Q" sort="Xu, Q" uniqKey="Xu Q" first="Q" last="Xu">Q. Xu</name></author><author><name sortKey="Wick, G" sort="Wick, G" uniqKey="Wick G" first="G" last="Wick">G. Wick</name></author></analytic><series><title level="j">Molecular medicine (Cambridge, Mass.)</title><idno type="ISSN">1076-1551</idno><imprint><date when="1999" type="published">1999</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Anti-Inflammatory Agents, Non-Steroidal (pharmacology)</term><term>Aspirin (pharmacology)</term><term>Cell Division (drug effects)</term><term>Cells, Cultured (drug effects)</term><term>Cells, Cultured (metabolism)</term><term>Chaperonin 60 (drug effects)</term><term>Chaperonin 60 (metabolism)</term><term>Chemokine CCL2 (metabolism)</term><term>Cyclosporine (pharmacology)</term><term>E-Selectin (drug effects)</term><term>E-Selectin (metabolism)</term><term>Endothelium, Vascular (cytology)</term><term>Endothelium, Vascular (drug effects)</term><term>Endothelium, Vascular (metabolism)</term><term>Female</term><term>HSP70 Heat-Shock Proteins (drug effects)</term><term>HSP70 Heat-Shock Proteins (metabolism)</term><term>Heat-Shock Proteins (drug effects)</term><term>Heat-Shock Proteins (metabolism)</term><term>Humans</term><term>Immunosuppressive Agents (pharmacology)</term><term>Indomethacin (pharmacology)</term><term>Intercellular Adhesion Molecule-1 (drug effects)</term><term>Intercellular Adhesion Molecule-1 (metabolism)</term><term>Lymphocytes (drug effects)</term><term>Lymphocytes (metabolism)</term><term>Male</term><term>NF-kappa B (drug effects)</term><term>NF-kappa B (genetics)</term><term>NF-kappa B (metabolism)</term><term>Transcription Factors (drug effects)</term><term>Transcription Factors (genetics)</term><term>Transcription Factors (metabolism)</term><term>Vascular Cell Adhesion Molecule-1 (drug effects)</term><term>Vascular Cell Adhesion Molecule-1 (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Chaperonin 60</term><term>E-Selectin</term><term>HSP70 Heat-Shock Proteins</term><term>Heat-Shock Proteins</term><term>Intercellular Adhesion Molecule-1</term><term>NF-kappa B</term><term>Transcription Factors</term><term>Vascular Cell Adhesion Molecule-1</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>NF-kappa B</term><term>Transcription Factors</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Chaperonin 60</term><term>Chemokine CCL2</term><term>E-Selectin</term><term>HSP70 Heat-Shock Proteins</term><term>Heat-Shock Proteins</term><term>Intercellular Adhesion Molecule-1</term><term>NF-kappa B</term><term>Transcription Factors</term><term>Vascular Cell Adhesion Molecule-1</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Anti-Inflammatory Agents, Non-Steroidal</term><term>Aspirin</term><term>Cyclosporine</term><term>Immunosuppressive Agents</term><term>Indomethacin</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Endothelium, Vascular</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Division</term><term>Cells, Cultured</term><term>Endothelium, Vascular</term><term>Lymphocytes</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Cells, Cultured</term><term>Endothelium, Vascular</term><term>Lymphocytes</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Female</term><term>Humans</term><term>Male</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Studies from our laboratory have shown that the earliest stages of atherosclerosis may be mediated by an autoimmune reaction against heat shock protein 60 (Hsp60). The interactions of Hsp60-specific T cells with arterial endothelial cells (EC) require expression of both Hsp60 and certain adhesion molecules shown to be induced simultaneously in EC by mechanical and other types of stress. Recently, it was shown that suppression of T cell-mediated immune responses by cyclosporin A (CyA) enhanced atherosclerotic lesion formation in mice. In contrast, aspirin was found to lower the risk of myocardial infarction in men. These conflicting observations may be due to different effects of anti-inflammatory agents on adhesion molecule and Hsp expression in EC, respectively.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">10203577</PMID><DateCompleted><Year>1999</Year><Month>06</Month><Day>11</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1076-1551</ISSN><JournalIssue CitedMedium="Print"><Volume>5</Volume><Issue>2</Issue><PubDate><Year>1999</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Molecular medicine (Cambridge, Mass.)</Title><ISOAbbreviation>Mol. Med.</ISOAbbreviation></Journal><ArticleTitle>Suppressive effects of anti-inflammatory agents on human endothelial cell activation and induction of heat shock proteins.</ArticleTitle><Pagination><MedlinePgn>117-28</MedlinePgn></Pagination><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Studies from our laboratory have shown that the earliest stages of atherosclerosis may be mediated by an autoimmune reaction against heat shock protein 60 (Hsp60). The interactions of Hsp60-specific T cells with arterial endothelial cells (EC) require expression of both Hsp60 and certain adhesion molecules shown to be induced simultaneously in EC by mechanical and other types of stress. Recently, it was shown that suppression of T cell-mediated immune responses by cyclosporin A (CyA) enhanced atherosclerotic lesion formation in mice. In contrast, aspirin was found to lower the risk of myocardial infarction in men. These conflicting observations may be due to different effects of anti-inflammatory agents on adhesion molecule and Hsp expression in EC, respectively.</AbstractText><AbstractText Label="MATERIAL AND METHODS" NlmCategory="METHODS">In the present study, we analyzed the effects of CyA, aspirin, and indomethacin on T cell proliferation using a proliferation assay. To explore the expression of adhesion molecules, monocyte chemoattractant protein-1 (MCP-1), and Hsp60 in human umbilical vein endothelial cells (HUVECs), Northern blot analyses were used. To examine the activation status of the transcription factors nuclear factor kappaB (NF-kappaB) and heat shock factor-1 (HSF-1), electrophoretic mobility shift assays were performed.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">With the exception of indomethacin, the used immunosuppressive and anti-inflammatory agents significantly inhibited T cell proliferation in response to influenza virus antigen in a dose-dependent manner. Interestingly, CyA and indomethacin did not suppress tumor necrosis factor-alpha (TNF-alpha)-induced adhesion molecule expression on HUVECs, whereas aspirin had an inhibitory effect. These observations correlated with the modulation of NF-kappaB activity in EC. All agents tested induced expression of Hsp60 6 hr after application. In addition, aspirin and indomethacin, but not CyA, induced Hsp70 expression in HUVECs that correlated with induction of HSF-1 activity.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Our results show that the tested agents (except indomethacin) are inhibitors of the T cell-mediated immune response, as expected, that aspirin is an effective suppressor of adhesion molecule expression, and that all three agents can induce Hsp60 in HUVECs. These data provide the molecular basis for the notion that (1) part of the anti-atherogenic effect of aspirin may be due to the prevention of the adhesion of sensitized T cells to stressed EC; (2) that part of the atherosclerosis-promoting effect of CyA may be due to its potential as an inducer of Hsp60 expression and its inability to down-regulate adhesion molecule expression on EC; and (3) that down-regulation of MCP-1 expression by aspirin may result in decreased recruitment of monocytes into the arterial intima beneath stressed EC.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Amberger</LastName><ForeName>A</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Institute for Biomedical Aging Research, Austrian Academy of Sciences, Innsbruck, Austria.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hala</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Saurwein-Teissl</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Metzler</LastName><ForeName>B</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Grubeck-Loebenstein</LastName><ForeName>B</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Xu</LastName><ForeName>Q</ForeName><Initials>Q</Initials></Author><Author ValidYN="Y"><LastName>Wick</LastName><ForeName>G</ForeName><Initials>G</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Mol Med</MedlineTA><NlmUniqueID>9501023</NlmUniqueID><ISSNLinking>1076-1551</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000894">Anti-Inflammatory Agents, Non-Steroidal</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018834">Chaperonin 60</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018932">Chemokine CCL2</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019040">E-Selectin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018840">HSP70 Heat-Shock Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006360">Heat-Shock Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007166">Immunosuppressive Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016328">NF-kappa B</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance 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Non-Steroidal</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001241" MajorTopicYN="N">Aspirin</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002455" MajorTopicYN="N">Cell Division</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018834" MajorTopicYN="N">Chaperonin 60</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018932" MajorTopicYN="N">Chemokine CCL2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016572" MajorTopicYN="N">Cyclosporine</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019040" MajorTopicYN="N">E-Selectin</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004730" MajorTopicYN="N">Endothelium, Vascular</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018840" MajorTopicYN="N">HSP70 Heat-Shock Proteins</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006360" MajorTopicYN="N">Heat-Shock Proteins</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007166" MajorTopicYN="N">Immunosuppressive Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007213" MajorTopicYN="N">Indomethacin</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018799" MajorTopicYN="N">Intercellular Adhesion Molecule-1</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008214" MajorTopicYN="N">Lymphocytes</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016328" MajorTopicYN="N">NF-kappa B</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014157" MajorTopicYN="N">Transcription Factors</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019010" MajorTopicYN="N">Vascular Cell Adhesion Molecule-1</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1999</Year><Month>4</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1999</Year><Month>4</Month><Day>16</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1999</Year><Month>4</Month><Day>16</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId 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