Interferon-γ induces apoptosis and expression of inflammation-related proteins in Chang conjunctival cells
The purpose of this study was to investigate the effect of interferon (IFN)gamma on cell viability, cell growth, and apoptosis and on expression of apoptotic and inflammation-related proteins in epithelial conjunctival cells in vitro. Some aspects of transduction pathways of IFNgamma-induced alterat...
Gespeichert in:
| Veröffentlicht in: | Investigative ophthalmology & visual science 1999-09, Vol.40 (10), p.2199-2212 |
|---|---|
| Hauptverfasser: | , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 2212 |
|---|---|
| container_issue | 10 |
| container_start_page | 2199 |
| container_title | Investigative ophthalmology & visual science |
| container_volume | 40 |
| creator | DE SAINT JEAN, M BRIGNOLE, F FELDMANN, G GOGUEL, A BAUDOUIN, C |
| description | The purpose of this study was to investigate the effect of interferon (IFN)gamma on cell viability, cell growth, and apoptosis and on expression of apoptotic and inflammation-related proteins in epithelial conjunctival cells in vitro. Some aspects of transduction pathways of IFNgamma-induced alterations were also investigated, especially the role of protein kinase C (PKC) and IFNgamma transcriptional factor STAT1.
A human conjunctival cell line was treated with different concentrations (30 and 300 U/ml) of human recombinant IFNgamma. After 24, 48, and 72 hours of treatment, cell viability and relative cell number were studied with 3-(4,5-dimethylthiazol-2yl)2,5-diphenyl tetrazolium bromide (MTT) and crystal violet colorimetric assays. The apoptotic process was sought by phase-contrast microscopy, 4',6'-diamidino-2-phenylindole dihydrochloride (DAPI) staining, and transmission electron microscopy and was confirmed by DNA electrophoresis and immunoblotting of poly(ADP-ribose) polymerase (PARP). The cell cycle and expression of apoptotic proteins Fas, bax, and p53; of inflammation-related proteins HLA-DR and intercellular adhesion molecule (ICAM)-1; and of IFNgamma signal-transducing factor STAT1 were evaluated by flow cytometry and/or western blot analysis. To investigate PKC-related transduction pathways, two PKC modulators, 12-O-tetradecanoyl-phorbol-13-acetate (TPA) and staurosporine, were applied for 3 hours, followed by IFNgamma treatment for 72 hours. Moreover, the effects of PKC depletion were studied after a 24-hour application of TPA, also followed by IFNgamma treatment for 72 hours. Then, Fas, ICAM-1, and HLA-DR expressions were studied by flow cytometry.
IFNgamma at 30 U/ml induced no change in cell cycle and in cell viability. Cell viability significantly decreased after 48 hours of treatment with 300 U/ml IFNgamma, associated with cell cycle alterations (decrease in number of cells in the S-M phase), apoptotic chromatin condensation and fragmentation, ladder pattern on DNA electrophoresis assay, and cleavage of PARP. Moreover, IFNgamma-treated cells overexpressed plasma membrane Fas, HLA-DR, and ICAM-1 in a dose- and time-dependent manner, and STAT1 in both nuclear and cytosolic cell fractions. Only 300 U/ml IFNgamma-treated cells overexpressed bax, whereas Bcl-2 and p53 proteins were not modified. HLA-DR and Fas were upregulated after addition of staurosporine or after PKC-depleting treatment and repressed with TPA. Staurosporine, PKC depletion |
| format | Article |
| fullrecord | <record><control><sourceid>pubmed_pasca</sourceid><recordid>TN_cdi_pubmed_primary_10476784</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>10476784</sourcerecordid><originalsourceid>FETCH-LOGICAL-p236t-6f828c913fe3257011026cf9c42fbef3d82605ad4879d85cf97bfbb6e8dc85893</originalsourceid><addsrcrecordid>eNpFkEtKBDEYhIMozjh6BcnCbSBJJ-n0UgYfAwNudD2k89CM6aRJMqLn8h6eyYCKq_qL-ij46wgsCecU8V52x2CJCRMIM8wW4KyUPcaUEIpPwYJg1otesiV43cRqs7M5RfT1CX00B20LVHOaayq-XdFA-z5nW4pPESbXGBfUNKnaPMo2qGoNnHOq1sfSUrh-UfEZ6hT3h6irf1MBahtCOQcnToViL351BZ5ubx7X92j7cLdZX2_RTDtRkXCSSj2QztmO8h4TgqnQbtCMutG6zkgqMFeGyX4wkrekH904CiuNllwO3Qpc_vTOh3GyZjdnP6n8sfv7ugFXv4AqWgWXVdS-_HNDa2kLfgNQfmSE</addsrcrecordid><sourcetype>Index Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Interferon-γ induces apoptosis and expression of inflammation-related proteins in Chang conjunctival cells</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><creator>DE SAINT JEAN, M ; BRIGNOLE, F ; FELDMANN, G ; GOGUEL, A ; BAUDOUIN, C</creator><creatorcontrib>DE SAINT JEAN, M ; BRIGNOLE, F ; FELDMANN, G ; GOGUEL, A ; BAUDOUIN, C</creatorcontrib><description>The purpose of this study was to investigate the effect of interferon (IFN)gamma on cell viability, cell growth, and apoptosis and on expression of apoptotic and inflammation-related proteins in epithelial conjunctival cells in vitro. Some aspects of transduction pathways of IFNgamma-induced alterations were also investigated, especially the role of protein kinase C (PKC) and IFNgamma transcriptional factor STAT1.
A human conjunctival cell line was treated with different concentrations (30 and 300 U/ml) of human recombinant IFNgamma. After 24, 48, and 72 hours of treatment, cell viability and relative cell number were studied with 3-(4,5-dimethylthiazol-2yl)2,5-diphenyl tetrazolium bromide (MTT) and crystal violet colorimetric assays. The apoptotic process was sought by phase-contrast microscopy, 4',6'-diamidino-2-phenylindole dihydrochloride (DAPI) staining, and transmission electron microscopy and was confirmed by DNA electrophoresis and immunoblotting of poly(ADP-ribose) polymerase (PARP). The cell cycle and expression of apoptotic proteins Fas, bax, and p53; of inflammation-related proteins HLA-DR and intercellular adhesion molecule (ICAM)-1; and of IFNgamma signal-transducing factor STAT1 were evaluated by flow cytometry and/or western blot analysis. To investigate PKC-related transduction pathways, two PKC modulators, 12-O-tetradecanoyl-phorbol-13-acetate (TPA) and staurosporine, were applied for 3 hours, followed by IFNgamma treatment for 72 hours. Moreover, the effects of PKC depletion were studied after a 24-hour application of TPA, also followed by IFNgamma treatment for 72 hours. Then, Fas, ICAM-1, and HLA-DR expressions were studied by flow cytometry.
IFNgamma at 30 U/ml induced no change in cell cycle and in cell viability. Cell viability significantly decreased after 48 hours of treatment with 300 U/ml IFNgamma, associated with cell cycle alterations (decrease in number of cells in the S-M phase), apoptotic chromatin condensation and fragmentation, ladder pattern on DNA electrophoresis assay, and cleavage of PARP. Moreover, IFNgamma-treated cells overexpressed plasma membrane Fas, HLA-DR, and ICAM-1 in a dose- and time-dependent manner, and STAT1 in both nuclear and cytosolic cell fractions. Only 300 U/ml IFNgamma-treated cells overexpressed bax, whereas Bcl-2 and p53 proteins were not modified. HLA-DR and Fas were upregulated after addition of staurosporine or after PKC-depleting treatment and repressed with TPA. Staurosporine, PKC depletion, and TPA all enhanced ICAM-1 expression.
In our model, IFNgamma induced expression of inflammatory molecules and apoptotic mediators, cell growth arrest, and apoptosis of Chang conjunctival cells. Moreover, our results suggest that activation of PKC is not involved in some IFNgamma cellular effects that possibly imply the upregulation and nuclear translocation of STAT1. IFNgamma-induced apoptosis could explain in part the recently reported coexistence of inflammation and programmed cell death in ocular surface inflammatory disorders such as Sjögren's syndrome.</description><identifier>ISSN: 0146-0404</identifier><identifier>EISSN: 1552-5783</identifier><identifier>PMID: 10476784</identifier><identifier>CODEN: IOVSDA</identifier><language>eng</language><publisher>Rockville, MD: Association for Research in Vision and Ophtalmology</publisher><subject>Apoptosis - drug effects ; bcl-2-Associated X Protein ; Biological and medical sciences ; Blotting, Western ; Cell Cycle - drug effects ; Cell Division - drug effects ; Cell Line ; Cell Survival - drug effects ; Conjunctiva - cytology ; Conjunctiva - drug effects ; Conjunctiva - metabolism ; Diseases of eyelid, conjunctiva and lacrimal tracts ; DNA-Binding Proteins - metabolism ; Dose-Response Relationship, Drug ; Epithelial Cells - cytology ; Epithelial Cells - drug effects ; Epithelial Cells - metabolism ; Fas Ligand Protein ; Flow Cytometry ; HLA-DR Antigens - metabolism ; Humans ; Intercellular Adhesion Molecule-1 - metabolism ; Interferon-gamma - pharmacology ; Medical sciences ; Membrane Glycoproteins - metabolism ; Ophthalmology ; Protein Kinase C - metabolism ; Proto-Oncogene Proteins - metabolism ; Proto-Oncogene Proteins c-bcl-2 ; Recombinant Proteins ; STAT1 Transcription Factor ; Staurosporine - pharmacology ; Tetradecanoylphorbol Acetate - pharmacology ; Time Factors ; Trans-Activators - metabolism ; Tumor Suppressor Protein p53 - metabolism</subject><ispartof>Investigative ophthalmology & visual science, 1999-09, Vol.40 (10), p.2199-2212</ispartof><rights>1999 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1958978$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10476784$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>DE SAINT JEAN, M</creatorcontrib><creatorcontrib>BRIGNOLE, F</creatorcontrib><creatorcontrib>FELDMANN, G</creatorcontrib><creatorcontrib>GOGUEL, A</creatorcontrib><creatorcontrib>BAUDOUIN, C</creatorcontrib><title>Interferon-γ induces apoptosis and expression of inflammation-related proteins in Chang conjunctival cells</title><title>Investigative ophthalmology & visual science</title><addtitle>Invest Ophthalmol Vis Sci</addtitle><description>The purpose of this study was to investigate the effect of interferon (IFN)gamma on cell viability, cell growth, and apoptosis and on expression of apoptotic and inflammation-related proteins in epithelial conjunctival cells in vitro. Some aspects of transduction pathways of IFNgamma-induced alterations were also investigated, especially the role of protein kinase C (PKC) and IFNgamma transcriptional factor STAT1.
A human conjunctival cell line was treated with different concentrations (30 and 300 U/ml) of human recombinant IFNgamma. After 24, 48, and 72 hours of treatment, cell viability and relative cell number were studied with 3-(4,5-dimethylthiazol-2yl)2,5-diphenyl tetrazolium bromide (MTT) and crystal violet colorimetric assays. The apoptotic process was sought by phase-contrast microscopy, 4',6'-diamidino-2-phenylindole dihydrochloride (DAPI) staining, and transmission electron microscopy and was confirmed by DNA electrophoresis and immunoblotting of poly(ADP-ribose) polymerase (PARP). The cell cycle and expression of apoptotic proteins Fas, bax, and p53; of inflammation-related proteins HLA-DR and intercellular adhesion molecule (ICAM)-1; and of IFNgamma signal-transducing factor STAT1 were evaluated by flow cytometry and/or western blot analysis. To investigate PKC-related transduction pathways, two PKC modulators, 12-O-tetradecanoyl-phorbol-13-acetate (TPA) and staurosporine, were applied for 3 hours, followed by IFNgamma treatment for 72 hours. Moreover, the effects of PKC depletion were studied after a 24-hour application of TPA, also followed by IFNgamma treatment for 72 hours. Then, Fas, ICAM-1, and HLA-DR expressions were studied by flow cytometry.
IFNgamma at 30 U/ml induced no change in cell cycle and in cell viability. Cell viability significantly decreased after 48 hours of treatment with 300 U/ml IFNgamma, associated with cell cycle alterations (decrease in number of cells in the S-M phase), apoptotic chromatin condensation and fragmentation, ladder pattern on DNA electrophoresis assay, and cleavage of PARP. Moreover, IFNgamma-treated cells overexpressed plasma membrane Fas, HLA-DR, and ICAM-1 in a dose- and time-dependent manner, and STAT1 in both nuclear and cytosolic cell fractions. Only 300 U/ml IFNgamma-treated cells overexpressed bax, whereas Bcl-2 and p53 proteins were not modified. HLA-DR and Fas were upregulated after addition of staurosporine or after PKC-depleting treatment and repressed with TPA. Staurosporine, PKC depletion, and TPA all enhanced ICAM-1 expression.
In our model, IFNgamma induced expression of inflammatory molecules and apoptotic mediators, cell growth arrest, and apoptosis of Chang conjunctival cells. Moreover, our results suggest that activation of PKC is not involved in some IFNgamma cellular effects that possibly imply the upregulation and nuclear translocation of STAT1. IFNgamma-induced apoptosis could explain in part the recently reported coexistence of inflammation and programmed cell death in ocular surface inflammatory disorders such as Sjögren's syndrome.</description><subject>Apoptosis - drug effects</subject><subject>bcl-2-Associated X Protein</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Cell Cycle - drug effects</subject><subject>Cell Division - drug effects</subject><subject>Cell Line</subject><subject>Cell Survival - drug effects</subject><subject>Conjunctiva - cytology</subject><subject>Conjunctiva - drug effects</subject><subject>Conjunctiva - metabolism</subject><subject>Diseases of eyelid, conjunctiva and lacrimal tracts</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Dose-Response Relationship, Drug</subject><subject>Epithelial Cells - cytology</subject><subject>Epithelial Cells - drug effects</subject><subject>Epithelial Cells - metabolism</subject><subject>Fas Ligand Protein</subject><subject>Flow Cytometry</subject><subject>HLA-DR Antigens - metabolism</subject><subject>Humans</subject><subject>Intercellular Adhesion Molecule-1 - metabolism</subject><subject>Interferon-gamma - pharmacology</subject><subject>Medical sciences</subject><subject>Membrane Glycoproteins - metabolism</subject><subject>Ophthalmology</subject><subject>Protein Kinase C - metabolism</subject><subject>Proto-Oncogene Proteins - metabolism</subject><subject>Proto-Oncogene Proteins c-bcl-2</subject><subject>Recombinant Proteins</subject><subject>STAT1 Transcription Factor</subject><subject>Staurosporine - pharmacology</subject><subject>Tetradecanoylphorbol Acetate - pharmacology</subject><subject>Time Factors</subject><subject>Trans-Activators - metabolism</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><issn>0146-0404</issn><issn>1552-5783</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkEtKBDEYhIMozjh6BcnCbSBJJ-n0UgYfAwNudD2k89CM6aRJMqLn8h6eyYCKq_qL-ij46wgsCecU8V52x2CJCRMIM8wW4KyUPcaUEIpPwYJg1otesiV43cRqs7M5RfT1CX00B20LVHOaayq-XdFA-z5nW4pPESbXGBfUNKnaPMo2qGoNnHOq1sfSUrh-UfEZ6hT3h6irf1MBahtCOQcnToViL351BZ5ubx7X92j7cLdZX2_RTDtRkXCSSj2QztmO8h4TgqnQbtCMutG6zkgqMFeGyX4wkrekH904CiuNllwO3Qpc_vTOh3GyZjdnP6n8sfv7ugFXv4AqWgWXVdS-_HNDa2kLfgNQfmSE</recordid><startdate>19990901</startdate><enddate>19990901</enddate><creator>DE SAINT JEAN, M</creator><creator>BRIGNOLE, F</creator><creator>FELDMANN, G</creator><creator>GOGUEL, A</creator><creator>BAUDOUIN, C</creator><general>Association for Research in Vision and Ophtalmology</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>19990901</creationdate><title>Interferon-γ induces apoptosis and expression of inflammation-related proteins in Chang conjunctival cells</title><author>DE SAINT JEAN, M ; BRIGNOLE, F ; FELDMANN, G ; GOGUEL, A ; BAUDOUIN, C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p236t-6f828c913fe3257011026cf9c42fbef3d82605ad4879d85cf97bfbb6e8dc85893</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Apoptosis - drug effects</topic><topic>bcl-2-Associated X Protein</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Cell Cycle - drug effects</topic><topic>Cell Division - drug effects</topic><topic>Cell Line</topic><topic>Cell Survival - drug effects</topic><topic>Conjunctiva - cytology</topic><topic>Conjunctiva - drug effects</topic><topic>Conjunctiva - metabolism</topic><topic>Diseases of eyelid, conjunctiva and lacrimal tracts</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Dose-Response Relationship, Drug</topic><topic>Epithelial Cells - cytology</topic><topic>Epithelial Cells - drug effects</topic><topic>Epithelial Cells - metabolism</topic><topic>Fas Ligand Protein</topic><topic>Flow Cytometry</topic><topic>HLA-DR Antigens - metabolism</topic><topic>Humans</topic><topic>Intercellular Adhesion Molecule-1 - metabolism</topic><topic>Interferon-gamma - pharmacology</topic><topic>Medical sciences</topic><topic>Membrane Glycoproteins - metabolism</topic><topic>Ophthalmology</topic><topic>Protein Kinase C - metabolism</topic><topic>Proto-Oncogene Proteins - metabolism</topic><topic>Proto-Oncogene Proteins c-bcl-2</topic><topic>Recombinant Proteins</topic><topic>STAT1 Transcription Factor</topic><topic>Staurosporine - pharmacology</topic><topic>Tetradecanoylphorbol Acetate - pharmacology</topic><topic>Time Factors</topic><topic>Trans-Activators - metabolism</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>DE SAINT JEAN, M</creatorcontrib><creatorcontrib>BRIGNOLE, F</creatorcontrib><creatorcontrib>FELDMANN, G</creatorcontrib><creatorcontrib>GOGUEL, A</creatorcontrib><creatorcontrib>BAUDOUIN, C</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Investigative ophthalmology & visual science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>DE SAINT JEAN, M</au><au>BRIGNOLE, F</au><au>FELDMANN, G</au><au>GOGUEL, A</au><au>BAUDOUIN, C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interferon-γ induces apoptosis and expression of inflammation-related proteins in Chang conjunctival cells</atitle><jtitle>Investigative ophthalmology & visual science</jtitle><addtitle>Invest Ophthalmol Vis Sci</addtitle><date>1999-09-01</date><risdate>1999</risdate><volume>40</volume><issue>10</issue><spage>2199</spage><epage>2212</epage><pages>2199-2212</pages><issn>0146-0404</issn><eissn>1552-5783</eissn><coden>IOVSDA</coden><abstract>The purpose of this study was to investigate the effect of interferon (IFN)gamma on cell viability, cell growth, and apoptosis and on expression of apoptotic and inflammation-related proteins in epithelial conjunctival cells in vitro. Some aspects of transduction pathways of IFNgamma-induced alterations were also investigated, especially the role of protein kinase C (PKC) and IFNgamma transcriptional factor STAT1.
A human conjunctival cell line was treated with different concentrations (30 and 300 U/ml) of human recombinant IFNgamma. After 24, 48, and 72 hours of treatment, cell viability and relative cell number were studied with 3-(4,5-dimethylthiazol-2yl)2,5-diphenyl tetrazolium bromide (MTT) and crystal violet colorimetric assays. The apoptotic process was sought by phase-contrast microscopy, 4',6'-diamidino-2-phenylindole dihydrochloride (DAPI) staining, and transmission electron microscopy and was confirmed by DNA electrophoresis and immunoblotting of poly(ADP-ribose) polymerase (PARP). The cell cycle and expression of apoptotic proteins Fas, bax, and p53; of inflammation-related proteins HLA-DR and intercellular adhesion molecule (ICAM)-1; and of IFNgamma signal-transducing factor STAT1 were evaluated by flow cytometry and/or western blot analysis. To investigate PKC-related transduction pathways, two PKC modulators, 12-O-tetradecanoyl-phorbol-13-acetate (TPA) and staurosporine, were applied for 3 hours, followed by IFNgamma treatment for 72 hours. Moreover, the effects of PKC depletion were studied after a 24-hour application of TPA, also followed by IFNgamma treatment for 72 hours. Then, Fas, ICAM-1, and HLA-DR expressions were studied by flow cytometry.
IFNgamma at 30 U/ml induced no change in cell cycle and in cell viability. Cell viability significantly decreased after 48 hours of treatment with 300 U/ml IFNgamma, associated with cell cycle alterations (decrease in number of cells in the S-M phase), apoptotic chromatin condensation and fragmentation, ladder pattern on DNA electrophoresis assay, and cleavage of PARP. Moreover, IFNgamma-treated cells overexpressed plasma membrane Fas, HLA-DR, and ICAM-1 in a dose- and time-dependent manner, and STAT1 in both nuclear and cytosolic cell fractions. Only 300 U/ml IFNgamma-treated cells overexpressed bax, whereas Bcl-2 and p53 proteins were not modified. HLA-DR and Fas were upregulated after addition of staurosporine or after PKC-depleting treatment and repressed with TPA. Staurosporine, PKC depletion, and TPA all enhanced ICAM-1 expression.
In our model, IFNgamma induced expression of inflammatory molecules and apoptotic mediators, cell growth arrest, and apoptosis of Chang conjunctival cells. Moreover, our results suggest that activation of PKC is not involved in some IFNgamma cellular effects that possibly imply the upregulation and nuclear translocation of STAT1. IFNgamma-induced apoptosis could explain in part the recently reported coexistence of inflammation and programmed cell death in ocular surface inflammatory disorders such as Sjögren's syndrome.</abstract><cop>Rockville, MD</cop><pub>Association for Research in Vision and Ophtalmology</pub><pmid>10476784</pmid><tpages>14</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0146-0404 |
| ispartof | Investigative ophthalmology & visual science, 1999-09, Vol.40 (10), p.2199-2212 |
| issn | 0146-0404 1552-5783 |
| language | eng |
| recordid | cdi_pubmed_primary_10476784 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Apoptosis - drug effects bcl-2-Associated X Protein Biological and medical sciences Blotting, Western Cell Cycle - drug effects Cell Division - drug effects Cell Line Cell Survival - drug effects Conjunctiva - cytology Conjunctiva - drug effects Conjunctiva - metabolism Diseases of eyelid, conjunctiva and lacrimal tracts DNA-Binding Proteins - metabolism Dose-Response Relationship, Drug Epithelial Cells - cytology Epithelial Cells - drug effects Epithelial Cells - metabolism Fas Ligand Protein Flow Cytometry HLA-DR Antigens - metabolism Humans Intercellular Adhesion Molecule-1 - metabolism Interferon-gamma - pharmacology Medical sciences Membrane Glycoproteins - metabolism Ophthalmology Protein Kinase C - metabolism Proto-Oncogene Proteins - metabolism Proto-Oncogene Proteins c-bcl-2 Recombinant Proteins STAT1 Transcription Factor Staurosporine - pharmacology Tetradecanoylphorbol Acetate - pharmacology Time Factors Trans-Activators - metabolism Tumor Suppressor Protein p53 - metabolism |
| title | Interferon-γ induces apoptosis and expression of inflammation-related proteins in Chang conjunctival cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-03T00%3A37%3A14IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-pubmed_pasca&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Interferon-%CE%B3%20induces%20apoptosis%20and%20expression%20of%20inflammation-related%20proteins%20in%20Chang%20conjunctival%20cells&rft.jtitle=Investigative%20ophthalmology%20&%20visual%20science&rft.au=DE%20SAINT%20JEAN,%20M&rft.date=1999-09-01&rft.volume=40&rft.issue=10&rft.spage=2199&rft.epage=2212&rft.pages=2199-2212&rft.issn=0146-0404&rft.eissn=1552-5783&rft.coden=IOVSDA&rft_id=info:doi/&rft_dat=%3Cpubmed_pasca%3E10476784%3C/pubmed_pasca%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_id=info:pmid/10476784&rfr_iscdi=true |