Preventing oxidative stress: a new role for XBP1
Antioxidant molecules reduce oxidative stress and protect cells from reactive oxygen species (ROS)-mediated cellular damage and probably the development of cancer. We have investigated the contribution of X-box-binding protein (XBP1), a major endoplasmic reticulum stress-linked transcriptional facto...
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| Veröffentlicht in: | Cell death and differentiation 2009-06, Vol.16 (6), p.847-857 |
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| creator | Liu, Y Adachi, M Zhao, S Hareyama, M Koong, A C Luo, Dan Rando, T A Imai, K Shinomura, Y |
| description | Antioxidant molecules reduce oxidative stress and protect cells from reactive oxygen species (ROS)-mediated cellular damage and probably the development of cancer. We have investigated the contribution of X-box-binding protein (XBP1), a major endoplasmic reticulum stress-linked transcriptional factor, to cellular resistance to oxidative stress. After exposure to hydrogen peroxide (H
2
O
2
) or a strong ROS inducer parthenolide, loss of mitochondrial membrane potential (MMP) and subsequent cell death occurred more extensively in XBP1-deficient cells than wild-type mouse embryonic fibroblast cells, whereas two other anticancer agents induced death similarly in both cells. In XBP1-deficient cells, H
2
O
2
exposure induced more extensive ROS generation and prolonged p38 phosphorylation, and expression of several antioxidant molecules including catalase was lower. Knockdown of XBP1 decreased catalase expression, enhanced ROS generation and MMP loss after H
2
O
2
exposure, but extrinsic catalase supply rescued them. Overexpression of XBP1 recovered catalase expression in XBP1-deficient cells and diminished ROS generation after H
2
O
2
exposure. Mutation analysis of the catalase promoter region suggests a pivotal role of CCAAT boxes, NF-Y-binding sites, for the XBP1-mediated enhancing effect. Taken together, these results indicate a protective role of XBP1 against oxidative stress, and its positive regulation of catalase expression may at least in part account for this function. |
| doi_str_mv | 10.1038/cdd.2009.14 |
| format | Article |
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2
O
2
) or a strong ROS inducer parthenolide, loss of mitochondrial membrane potential (MMP) and subsequent cell death occurred more extensively in XBP1-deficient cells than wild-type mouse embryonic fibroblast cells, whereas two other anticancer agents induced death similarly in both cells. In XBP1-deficient cells, H
2
O
2
exposure induced more extensive ROS generation and prolonged p38 phosphorylation, and expression of several antioxidant molecules including catalase was lower. Knockdown of XBP1 decreased catalase expression, enhanced ROS generation and MMP loss after H
2
O
2
exposure, but extrinsic catalase supply rescued them. Overexpression of XBP1 recovered catalase expression in XBP1-deficient cells and diminished ROS generation after H
2
O
2
exposure. Mutation analysis of the catalase promoter region suggests a pivotal role of CCAAT boxes, NF-Y-binding sites, for the XBP1-mediated enhancing effect. Taken together, these results indicate a protective role of XBP1 against oxidative stress, and its positive regulation of catalase expression may at least in part account for this function.</description><identifier>ISSN: 1350-9047</identifier><identifier>EISSN: 1476-5403</identifier><identifier>DOI: 10.1038/cdd.2009.14</identifier><identifier>PMID: 19247368</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Animals ; Antioxidants ; Apoptosis ; Biochemistry ; Biomedical and Life Sciences ; Cancer ; Catalase - metabolism ; Cell Biology ; Cell Cycle Analysis ; Cell death ; Cell Line ; DNA-Binding Proteins - deficiency ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - physiology ; Endoplasmic reticulum ; Endoplasmic Reticulum - metabolism ; Fibroblasts - metabolism ; Gene expression ; Gene Knockdown Techniques ; HeLa Cells ; Homeostasis ; Humans ; Hydrogen Peroxide - pharmacology ; Internal medicine ; Life Sciences ; Medicine ; Mice ; Oncology ; original-paper ; Oxidative Stress ; p38 Mitogen-Activated Protein Kinases - metabolism ; Phosphorylation ; Proteins ; Radiation ; Reactive Oxygen Species - metabolism ; Regulatory Factor X Transcription Factors ; RNA, Small Interfering - metabolism ; Stem Cells ; Transcription Factors - deficiency ; Transcription Factors - genetics ; Transcription Factors - physiology ; X-Box Binding Protein 1</subject><ispartof>Cell death and differentiation, 2009-06, Vol.16 (6), p.847-857</ispartof><rights>Macmillan Publishers Limited 2009</rights><rights>Copyright Nature Publishing Group Jun 2009</rights><rights>2009 Macmillan Publishers Limited All rights reserved 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-n251t-d52366d8aa120ba2360aef46833b94e2275becf000c62875b581fee47b7648023</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,315,781,785,886,27929,27930</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19247368$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Y</creatorcontrib><creatorcontrib>Adachi, M</creatorcontrib><creatorcontrib>Zhao, S</creatorcontrib><creatorcontrib>Hareyama, M</creatorcontrib><creatorcontrib>Koong, A C</creatorcontrib><creatorcontrib>Luo, Dan</creatorcontrib><creatorcontrib>Rando, T A</creatorcontrib><creatorcontrib>Imai, K</creatorcontrib><creatorcontrib>Shinomura, Y</creatorcontrib><title>Preventing oxidative stress: a new role for XBP1</title><title>Cell death and differentiation</title><addtitle>Cell Death Differ</addtitle><addtitle>Cell Death Differ</addtitle><description>Antioxidant molecules reduce oxidative stress and protect cells from reactive oxygen species (ROS)-mediated cellular damage and probably the development of cancer. We have investigated the contribution of X-box-binding protein (XBP1), a major endoplasmic reticulum stress-linked transcriptional factor, to cellular resistance to oxidative stress. After exposure to hydrogen peroxide (H
2
O
2
) or a strong ROS inducer parthenolide, loss of mitochondrial membrane potential (MMP) and subsequent cell death occurred more extensively in XBP1-deficient cells than wild-type mouse embryonic fibroblast cells, whereas two other anticancer agents induced death similarly in both cells. In XBP1-deficient cells, H
2
O
2
exposure induced more extensive ROS generation and prolonged p38 phosphorylation, and expression of several antioxidant molecules including catalase was lower. Knockdown of XBP1 decreased catalase expression, enhanced ROS generation and MMP loss after H
2
O
2
exposure, but extrinsic catalase supply rescued them. Overexpression of XBP1 recovered catalase expression in XBP1-deficient cells and diminished ROS generation after H
2
O
2
exposure. Mutation analysis of the catalase promoter region suggests a pivotal role of CCAAT boxes, NF-Y-binding sites, for the XBP1-mediated enhancing effect. Taken together, these results indicate a protective role of XBP1 against oxidative stress, and its positive regulation of catalase expression may at least in part account for this function.</description><subject>Animals</subject><subject>Antioxidants</subject><subject>Apoptosis</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cancer</subject><subject>Catalase - metabolism</subject><subject>Cell Biology</subject><subject>Cell Cycle Analysis</subject><subject>Cell death</subject><subject>Cell Line</subject><subject>DNA-Binding Proteins - deficiency</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - physiology</subject><subject>Endoplasmic reticulum</subject><subject>Endoplasmic Reticulum - metabolism</subject><subject>Fibroblasts - metabolism</subject><subject>Gene expression</subject><subject>Gene Knockdown Techniques</subject><subject>HeLa Cells</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Hydrogen Peroxide - pharmacology</subject><subject>Internal medicine</subject><subject>Life Sciences</subject><subject>Medicine</subject><subject>Mice</subject><subject>Oncology</subject><subject>original-paper</subject><subject>Oxidative Stress</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Phosphorylation</subject><subject>Proteins</subject><subject>Radiation</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Regulatory Factor X Transcription Factors</subject><subject>RNA, Small Interfering - metabolism</subject><subject>Stem Cells</subject><subject>Transcription Factors - deficiency</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - physiology</subject><subject>X-Box Binding Protein 1</subject><issn>1350-9047</issn><issn>1476-5403</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNpVkEtPwzAQhC0EoqVw4g4RZ1L8iu1wQIKKl1SJHkDiZjnJpqRqnWInAf49rloKnHZX-2lmNAgdEzwkmKmLvCiGFON0SPgO6hMuRZxwzHbDzhIcp5jLHjrwfoYxFjIV-6hHUsolE6qP8MRBB7ap7DSqP6vCNFUHkW8ceH8ZmcjCR-TqOURl7aLXmwk5RHulmXs42swBerm7fR49xOOn-8fR9Ti2NCFNXCSUCVEoYwjFmQkHNlByoRjLUg6UyiSDvAyRckFVOBJFSgAuMym4wpQN0NVad9lmCyjykNGZuV66amHcl65Npf9_bPWmp3WnqaKCBJ8BOtsIuPq9Bd_oWd06GzJrSqRkwToN0Mlfl638T0EBOF8DPrzsFNyvCsF61b8O_etV_5rwgJ-ucWua1sFWLzArJBDfoXt_IA</recordid><startdate>20090601</startdate><enddate>20090601</enddate><creator>Liu, Y</creator><creator>Adachi, M</creator><creator>Zhao, S</creator><creator>Hareyama, M</creator><creator>Koong, A C</creator><creator>Luo, Dan</creator><creator>Rando, T A</creator><creator>Imai, K</creator><creator>Shinomura, Y</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>3V.</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</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>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>20090601</creationdate><title>Preventing oxidative stress: a new role for XBP1</title><author>Liu, Y ; Adachi, M ; Zhao, S ; Hareyama, M ; Koong, A C ; Luo, Dan ; Rando, T A ; Imai, K ; Shinomura, Y</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-n251t-d52366d8aa120ba2360aef46833b94e2275becf000c62875b581fee47b7648023</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>Antioxidants</topic><topic>Apoptosis</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Cancer</topic><topic>Catalase - metabolism</topic><topic>Cell Biology</topic><topic>Cell Cycle Analysis</topic><topic>Cell death</topic><topic>Cell Line</topic><topic>DNA-Binding Proteins - deficiency</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - physiology</topic><topic>Endoplasmic reticulum</topic><topic>Endoplasmic Reticulum - metabolism</topic><topic>Fibroblasts - metabolism</topic><topic>Gene expression</topic><topic>Gene Knockdown Techniques</topic><topic>HeLa Cells</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>Hydrogen Peroxide - pharmacology</topic><topic>Internal medicine</topic><topic>Life Sciences</topic><topic>Medicine</topic><topic>Mice</topic><topic>Oncology</topic><topic>original-paper</topic><topic>Oxidative Stress</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Phosphorylation</topic><topic>Proteins</topic><topic>Radiation</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Regulatory Factor X Transcription Factors</topic><topic>RNA, Small Interfering - metabolism</topic><topic>Stem Cells</topic><topic>Transcription Factors - deficiency</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - physiology</topic><topic>X-Box Binding Protein 1</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Y</creatorcontrib><creatorcontrib>Adachi, M</creatorcontrib><creatorcontrib>Zhao, S</creatorcontrib><creatorcontrib>Hareyama, M</creatorcontrib><creatorcontrib>Koong, A C</creatorcontrib><creatorcontrib>Luo, Dan</creatorcontrib><creatorcontrib>Rando, T A</creatorcontrib><creatorcontrib>Imai, K</creatorcontrib><creatorcontrib>Shinomura, Y</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>Proquest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell death and differentiation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Y</au><au>Adachi, M</au><au>Zhao, S</au><au>Hareyama, M</au><au>Koong, A C</au><au>Luo, Dan</au><au>Rando, T A</au><au>Imai, K</au><au>Shinomura, Y</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Preventing oxidative stress: a new role for XBP1</atitle><jtitle>Cell death and differentiation</jtitle><stitle>Cell Death Differ</stitle><addtitle>Cell Death Differ</addtitle><date>2009-06-01</date><risdate>2009</risdate><volume>16</volume><issue>6</issue><spage>847</spage><epage>857</epage><pages>847-857</pages><issn>1350-9047</issn><eissn>1476-5403</eissn><abstract>Antioxidant molecules reduce oxidative stress and protect cells from reactive oxygen species (ROS)-mediated cellular damage and probably the development of cancer. We have investigated the contribution of X-box-binding protein (XBP1), a major endoplasmic reticulum stress-linked transcriptional factor, to cellular resistance to oxidative stress. After exposure to hydrogen peroxide (H
2
O
2
) or a strong ROS inducer parthenolide, loss of mitochondrial membrane potential (MMP) and subsequent cell death occurred more extensively in XBP1-deficient cells than wild-type mouse embryonic fibroblast cells, whereas two other anticancer agents induced death similarly in both cells. In XBP1-deficient cells, H
2
O
2
exposure induced more extensive ROS generation and prolonged p38 phosphorylation, and expression of several antioxidant molecules including catalase was lower. Knockdown of XBP1 decreased catalase expression, enhanced ROS generation and MMP loss after H
2
O
2
exposure, but extrinsic catalase supply rescued them. Overexpression of XBP1 recovered catalase expression in XBP1-deficient cells and diminished ROS generation after H
2
O
2
exposure. Mutation analysis of the catalase promoter region suggests a pivotal role of CCAAT boxes, NF-Y-binding sites, for the XBP1-mediated enhancing effect. Taken together, these results indicate a protective role of XBP1 against oxidative stress, and its positive regulation of catalase expression may at least in part account for this function.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>19247368</pmid><doi>10.1038/cdd.2009.14</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
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| ispartof | Cell death and differentiation, 2009-06, Vol.16 (6), p.847-857 |
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| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2826168 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Animals Antioxidants Apoptosis Biochemistry Biomedical and Life Sciences Cancer Catalase - metabolism Cell Biology Cell Cycle Analysis Cell death Cell Line DNA-Binding Proteins - deficiency DNA-Binding Proteins - genetics DNA-Binding Proteins - physiology Endoplasmic reticulum Endoplasmic Reticulum - metabolism Fibroblasts - metabolism Gene expression Gene Knockdown Techniques HeLa Cells Homeostasis Humans Hydrogen Peroxide - pharmacology Internal medicine Life Sciences Medicine Mice Oncology original-paper Oxidative Stress p38 Mitogen-Activated Protein Kinases - metabolism Phosphorylation Proteins Radiation Reactive Oxygen Species - metabolism Regulatory Factor X Transcription Factors RNA, Small Interfering - metabolism Stem Cells Transcription Factors - deficiency Transcription Factors - genetics Transcription Factors - physiology X-Box Binding Protein 1 |
| title | Preventing oxidative stress: a new role for XBP1 |
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