IFI6 Inhibits Apoptosis via Mitochondrial-Dependent Pathway in Dengue Virus 2 Infected Vascular Endothelial Cells
Dengue hemorrhagic fever (DHF)/Dengue shock syndrome (DSS) is a fatal infectious disease that demands an effective treatment. Interferon (IFN)-stimulated genes (ISGs) induced by dengue virus (DENV) exert antiviral effects. Among ISGs, IFN-α inducible gene 6 (IFI6) was increased in DENV infected huma...
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| creator | Qi, Yiming Li, Ying Zhang, Yingke Zhang, Lin Wang, Zilian Zhang, Xuzhi Gui, Lian Huang, Junqi |
| description | Dengue hemorrhagic fever (DHF)/Dengue shock syndrome (DSS) is a fatal infectious disease that demands an effective treatment. Interferon (IFN)-stimulated genes (ISGs) induced by dengue virus (DENV) exert antiviral effects. Among ISGs, IFN-α inducible gene 6 (IFI6) was increased in DENV infected human umbilical vascular endothelial cells (HUVECs) by microarray analysis in our previous study. However, its function is incompletely understood. In this study, we confirmed that IFI6 was markedly induced in DENV infection of both primary HUVECs and EA.hy926 cell lines. Recombinant EA.hy926 cell lines in which IFI6 was either over-expressed (IFI6+/+) or knocked-down (IFI6-/-) were generated. The activation of caspase-3 and intrinsic apoptosis-related protein caspase-9 were down-regulated in IFI6+/+ but up-regulated in IFI6-/- cells at 24-48 hrs post-infection. After incubation with DENV for 48 hrs, the mitochondrial membrane potential (Δψ(m)) was more stable in IFI6+/+ cells but reduced in IFI6-/- cells, as assayed by fluorescence staining with JC-1. We observed that Bcl-2 expression was increased in IFI6+/+ and decreased in IFI6-/- cells. By contrast, Bax expression was decreased in IFI6+/+ and increased in IFI6-/- cells. It is presumed that the anti-apoptotic function of IFI6 is expressed by regulating the rheostatic balance between bcl-2/bax expression and inhibition of Δψ(m) depolarization during DENV infection of vascular endothelial cells(VECs). In addition, the pro-apoptotic protein X-linked Inhibitor of Apoptosis (XIAP)-Associated Factor 1(XAF1) expression had been reported to be up-regulated and led to the induction of apoptosis in DENV2-infected VECs,but the relationship between XAF1 and IFI6 dengue virus-induced apoptosis in VECs warrants further study. |
| doi_str_mv | 10.1371/journal.pone.0132743 |
| format | Article |
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Interferon (IFN)-stimulated genes (ISGs) induced by dengue virus (DENV) exert antiviral effects. Among ISGs, IFN-α inducible gene 6 (IFI6) was increased in DENV infected human umbilical vascular endothelial cells (HUVECs) by microarray analysis in our previous study. However, its function is incompletely understood. In this study, we confirmed that IFI6 was markedly induced in DENV infection of both primary HUVECs and EA.hy926 cell lines. Recombinant EA.hy926 cell lines in which IFI6 was either over-expressed (IFI6+/+) or knocked-down (IFI6-/-) were generated. The activation of caspase-3 and intrinsic apoptosis-related protein caspase-9 were down-regulated in IFI6+/+ but up-regulated in IFI6-/- cells at 24-48 hrs post-infection. After incubation with DENV for 48 hrs, the mitochondrial membrane potential (Δψ(m)) was more stable in IFI6+/+ cells but reduced in IFI6-/- cells, as assayed by fluorescence staining with JC-1. We observed that Bcl-2 expression was increased in IFI6+/+ and decreased in IFI6-/- cells. By contrast, Bax expression was decreased in IFI6+/+ and increased in IFI6-/- cells. It is presumed that the anti-apoptotic function of IFI6 is expressed by regulating the rheostatic balance between bcl-2/bax expression and inhibition of Δψ(m) depolarization during DENV infection of vascular endothelial cells(VECs). In addition, the pro-apoptotic protein X-linked Inhibitor of Apoptosis (XIAP)-Associated Factor 1(XAF1) expression had been reported to be up-regulated and led to the induction of apoptosis in DENV2-infected VECs,but the relationship between XAF1 and IFI6 dengue virus-induced apoptosis in VECs warrants further study.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0132743</identifier><identifier>PMID: 26244642</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Apoptosis ; Apoptosis - genetics ; Bax protein ; Bcl-2 protein ; bcl-2-Associated X Protein - genetics ; bcl-2-Associated X Protein - metabolism ; Biological response modifiers ; Biotechnology ; Care and treatment ; Caspase ; Caspase-3 ; Caspase-9 ; Cell Line ; Cell lines ; Dengue - virology ; Dengue fever ; Dengue hemorrhagic fever ; Dengue Virus ; Depolarization ; Diagnosis ; DNA microarrays ; Down-Regulation ; Endothelial cells ; Endothelial Cells - metabolism ; Endothelial Cells - virology ; Endothelium ; Endothelium, Vascular - metabolism ; Endothelium, Vascular - virology ; Fever ; Fluorescence ; Genomics ; Health aspects ; Human Umbilical Vein Endothelial Cells - drug effects ; Human Umbilical Vein Endothelial Cells - metabolism ; Human Umbilical Vein Endothelial Cells - virology ; Humans ; Incubation ; Infections ; Infectious diseases ; Interferon ; Kinases ; Medical treatment ; Membrane potential ; Mitochondria ; Mitochondria - genetics ; Mitochondria - metabolism ; Mitochondrial Proteins - genetics ; Mitochondrial Proteins - metabolism ; Protein X ; Proteins ; Proto-Oncogene Proteins c-bcl-2 - genetics ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; Risk factors ; Signal Transduction - genetics ; Tropical diseases ; Up-Regulation ; Vector-borne diseases ; Viral diseases ; Viruses ; X-Linked Inhibitor of Apoptosis Protein - genetics ; X-Linked Inhibitor of Apoptosis Protein - metabolism ; XIAP protein ; α-Interferon</subject><ispartof>PloS one, 2015-08, Vol.10 (8), p.e0132743-e0132743</ispartof><rights>COPYRIGHT 2015 Public Library of Science</rights><rights>2015 Qi et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2015 Qi et al 2015 Qi et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-cfe723c1776bdb6fb8ae0865af722dcd202c641004180c1b0dd85a6fc0c5d0523</citedby><cites>FETCH-LOGICAL-c758t-cfe723c1776bdb6fb8ae0865af722dcd202c641004180c1b0dd85a6fc0c5d0523</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4526556/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4526556/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79343,79344</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26244642$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Jin, Xia</contributor><creatorcontrib>Qi, Yiming</creatorcontrib><creatorcontrib>Li, Ying</creatorcontrib><creatorcontrib>Zhang, Yingke</creatorcontrib><creatorcontrib>Zhang, Lin</creatorcontrib><creatorcontrib>Wang, Zilian</creatorcontrib><creatorcontrib>Zhang, Xuzhi</creatorcontrib><creatorcontrib>Gui, Lian</creatorcontrib><creatorcontrib>Huang, Junqi</creatorcontrib><title>IFI6 Inhibits Apoptosis via Mitochondrial-Dependent Pathway in Dengue Virus 2 Infected Vascular Endothelial Cells</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Dengue hemorrhagic fever (DHF)/Dengue shock syndrome (DSS) is a fatal infectious disease that demands an effective treatment. Interferon (IFN)-stimulated genes (ISGs) induced by dengue virus (DENV) exert antiviral effects. Among ISGs, IFN-α inducible gene 6 (IFI6) was increased in DENV infected human umbilical vascular endothelial cells (HUVECs) by microarray analysis in our previous study. However, its function is incompletely understood. In this study, we confirmed that IFI6 was markedly induced in DENV infection of both primary HUVECs and EA.hy926 cell lines. Recombinant EA.hy926 cell lines in which IFI6 was either over-expressed (IFI6+/+) or knocked-down (IFI6-/-) were generated. The activation of caspase-3 and intrinsic apoptosis-related protein caspase-9 were down-regulated in IFI6+/+ but up-regulated in IFI6-/- cells at 24-48 hrs post-infection. After incubation with DENV for 48 hrs, the mitochondrial membrane potential (Δψ(m)) was more stable in IFI6+/+ cells but reduced in IFI6-/- cells, as assayed by fluorescence staining with JC-1. We observed that Bcl-2 expression was increased in IFI6+/+ and decreased in IFI6-/- cells. By contrast, Bax expression was decreased in IFI6+/+ and increased in IFI6-/- cells. It is presumed that the anti-apoptotic function of IFI6 is expressed by regulating the rheostatic balance between bcl-2/bax expression and inhibition of Δψ(m) depolarization during DENV infection of vascular endothelial cells(VECs). In addition, the pro-apoptotic protein X-linked Inhibitor of Apoptosis (XIAP)-Associated Factor 1(XAF1) expression had been reported to be up-regulated and led to the induction of apoptosis in DENV2-infected VECs,but the relationship between XAF1 and IFI6 dengue virus-induced apoptosis in VECs warrants further study.</description><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Bax protein</subject><subject>Bcl-2 protein</subject><subject>bcl-2-Associated X Protein - genetics</subject><subject>bcl-2-Associated X Protein - metabolism</subject><subject>Biological response modifiers</subject><subject>Biotechnology</subject><subject>Care and treatment</subject><subject>Caspase</subject><subject>Caspase-3</subject><subject>Caspase-9</subject><subject>Cell Line</subject><subject>Cell lines</subject><subject>Dengue - virology</subject><subject>Dengue fever</subject><subject>Dengue hemorrhagic fever</subject><subject>Dengue Virus</subject><subject>Depolarization</subject><subject>Diagnosis</subject><subject>DNA microarrays</subject><subject>Down-Regulation</subject><subject>Endothelial cells</subject><subject>Endothelial Cells - metabolism</subject><subject>Endothelial Cells - virology</subject><subject>Endothelium</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Endothelium, Vascular - virology</subject><subject>Fever</subject><subject>Fluorescence</subject><subject>Genomics</subject><subject>Health aspects</subject><subject>Human Umbilical Vein Endothelial Cells - drug effects</subject><subject>Human Umbilical Vein Endothelial Cells - metabolism</subject><subject>Human Umbilical Vein Endothelial Cells - virology</subject><subject>Humans</subject><subject>Incubation</subject><subject>Infections</subject><subject>Infectious diseases</subject><subject>Interferon</subject><subject>Kinases</subject><subject>Medical treatment</subject><subject>Membrane potential</subject><subject>Mitochondria</subject><subject>Mitochondria - genetics</subject><subject>Mitochondria - metabolism</subject><subject>Mitochondrial Proteins - genetics</subject><subject>Mitochondrial Proteins - metabolism</subject><subject>Protein X</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-bcl-2 - genetics</subject><subject>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject><subject>Risk factors</subject><subject>Signal Transduction - genetics</subject><subject>Tropical diseases</subject><subject>Up-Regulation</subject><subject>Vector-borne diseases</subject><subject>Viral diseases</subject><subject>Viruses</subject><subject>X-Linked Inhibitor of Apoptosis Protein - genetics</subject><subject>X-Linked Inhibitor of Apoptosis Protein - metabolism</subject><subject>XIAP protein</subject><subject>α-Interferon</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNk11v0zAUhiMEYmPwDxBEQkJw0eKv2MnNpKrbINLQEB-9tRzbaVyldhY7g_173DWbGrQLlItEznMe2699kuQ1BHOIGfy0cUNvRTvvnNVzADFiBD9JjmGB0YwigJ8efB8lL7zfAJDhnNLnyRGiiBBK0HFyXV6UNC1tYyoTfLroXBecNz69MSL9aoKTjbOqN6KdnelOW6VtSL-J0PwWt6mx6Zm260GnK9MPPkVRVGsZtEpXwsuhFX16bpULjW6jIV3qtvUvk2e1aL1-Nb5Pkl8X5z-XX2aXV5_L5eJyJlmWh5msNUNYQsZopSpaV7nQIKeZqBlCSioEkKQEAkBgDiSsgFJ5JmgtgcwUyBA-Sd7uvV3rPB_T8hwyAPOCMUIiUe4J5cSGd73Ziv6WO2H43YDr11z0wchWc1YhXAtJYYZqoouq0DCKZFFDJKTEMLpOx9mGaquVjDH1op1Ip3-safja3XCSIZplNAo-jILeXQ_aB741XsbAhNVuuFs3oqQoMhbRd_-gj-9upNYibsDY2sV55U7KFwQjWiCWZ5GaP0LFR-mtkfFq1SaOTwo-TgoiE_SfsBaD97z88f3_2avVlH1_wDZatKHxrh2CcdZPQbIHZe-873X9EDIEfNcZ92nwXWfwsTNi2ZvDA3ooum8F_BcIwAjA</recordid><startdate>20150805</startdate><enddate>20150805</enddate><creator>Qi, Yiming</creator><creator>Li, Ying</creator><creator>Zhang, Yingke</creator><creator>Zhang, Lin</creator><creator>Wang, Zilian</creator><creator>Zhang, Xuzhi</creator><creator>Gui, Lian</creator><creator>Huang, Junqi</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20150805</creationdate><title>IFI6 Inhibits Apoptosis via Mitochondrial-Dependent Pathway in Dengue Virus 2 Infected Vascular Endothelial Cells</title><author>Qi, Yiming ; Li, Ying ; Zhang, Yingke ; Zhang, Lin ; Wang, Zilian ; Zhang, Xuzhi ; Gui, Lian ; Huang, Junqi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c758t-cfe723c1776bdb6fb8ae0865af722dcd202c641004180c1b0dd85a6fc0c5d0523</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Apoptosis</topic><topic>Apoptosis - 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Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Qi, Yiming</au><au>Li, Ying</au><au>Zhang, Yingke</au><au>Zhang, Lin</au><au>Wang, Zilian</au><au>Zhang, Xuzhi</au><au>Gui, Lian</au><au>Huang, Junqi</au><au>Jin, Xia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>IFI6 Inhibits Apoptosis via Mitochondrial-Dependent Pathway in Dengue Virus 2 Infected Vascular Endothelial Cells</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2015-08-05</date><risdate>2015</risdate><volume>10</volume><issue>8</issue><spage>e0132743</spage><epage>e0132743</epage><pages>e0132743-e0132743</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Dengue hemorrhagic fever (DHF)/Dengue shock syndrome (DSS) is a fatal infectious disease that demands an effective treatment. Interferon (IFN)-stimulated genes (ISGs) induced by dengue virus (DENV) exert antiviral effects. Among ISGs, IFN-α inducible gene 6 (IFI6) was increased in DENV infected human umbilical vascular endothelial cells (HUVECs) by microarray analysis in our previous study. However, its function is incompletely understood. In this study, we confirmed that IFI6 was markedly induced in DENV infection of both primary HUVECs and EA.hy926 cell lines. Recombinant EA.hy926 cell lines in which IFI6 was either over-expressed (IFI6+/+) or knocked-down (IFI6-/-) were generated. The activation of caspase-3 and intrinsic apoptosis-related protein caspase-9 were down-regulated in IFI6+/+ but up-regulated in IFI6-/- cells at 24-48 hrs post-infection. After incubation with DENV for 48 hrs, the mitochondrial membrane potential (Δψ(m)) was more stable in IFI6+/+ cells but reduced in IFI6-/- cells, as assayed by fluorescence staining with JC-1. We observed that Bcl-2 expression was increased in IFI6+/+ and decreased in IFI6-/- cells. By contrast, Bax expression was decreased in IFI6+/+ and increased in IFI6-/- cells. It is presumed that the anti-apoptotic function of IFI6 is expressed by regulating the rheostatic balance between bcl-2/bax expression and inhibition of Δψ(m) depolarization during DENV infection of vascular endothelial cells(VECs). In addition, the pro-apoptotic protein X-linked Inhibitor of Apoptosis (XIAP)-Associated Factor 1(XAF1) expression had been reported to be up-regulated and led to the induction of apoptosis in DENV2-infected VECs,but the relationship between XAF1 and IFI6 dengue virus-induced apoptosis in VECs warrants further study.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>26244642</pmid><doi>10.1371/journal.pone.0132743</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2015-08, Vol.10 (8), p.e0132743-e0132743 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1701897744 |
| source | Public Library of Science (PLoS) Journals Open Access; MEDLINE; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Apoptosis Apoptosis - genetics Bax protein Bcl-2 protein bcl-2-Associated X Protein - genetics bcl-2-Associated X Protein - metabolism Biological response modifiers Biotechnology Care and treatment Caspase Caspase-3 Caspase-9 Cell Line Cell lines Dengue - virology Dengue fever Dengue hemorrhagic fever Dengue Virus Depolarization Diagnosis DNA microarrays Down-Regulation Endothelial cells Endothelial Cells - metabolism Endothelial Cells - virology Endothelium Endothelium, Vascular - metabolism Endothelium, Vascular - virology Fever Fluorescence Genomics Health aspects Human Umbilical Vein Endothelial Cells - drug effects Human Umbilical Vein Endothelial Cells - metabolism Human Umbilical Vein Endothelial Cells - virology Humans Incubation Infections Infectious diseases Interferon Kinases Medical treatment Membrane potential Mitochondria Mitochondria - genetics Mitochondria - metabolism Mitochondrial Proteins - genetics Mitochondrial Proteins - metabolism Protein X Proteins Proto-Oncogene Proteins c-bcl-2 - genetics Proto-Oncogene Proteins c-bcl-2 - metabolism Risk factors Signal Transduction - genetics Tropical diseases Up-Regulation Vector-borne diseases Viral diseases Viruses X-Linked Inhibitor of Apoptosis Protein - genetics X-Linked Inhibitor of Apoptosis Protein - metabolism XIAP protein α-Interferon |
| title | IFI6 Inhibits Apoptosis via Mitochondrial-Dependent Pathway in Dengue Virus 2 Infected Vascular Endothelial Cells |
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