Loading…
Vitamin D3–Upregulated Protein-1 (VDUP-1) Regulates Redox-Dependent Vascular Smooth Muscle Cell Proliferation Through Interaction With Thioredoxin
ABSTRACT—Reactive oxygen species are important cellular signaling molecules, and thioredoxin (TRX) is a key regulator of cellular redox balance. We investigated the interaction of TRX with its endogenous inhibitor, vitamin D3–upregulated protein (VDUP)-1, in human aortic smooth muscle cells (SMCs)....
Saved in:
| Published in: | Circulation research 2002-10, Vol.91 (8), p.689-695 |
|---|---|
| Main Authors: | , , , , |
| Format: | Article |
| Language: | English |
| Subjects: | |
| Online Access: | Get full text |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| cited_by | |
|---|---|
| cites | |
| container_end_page | 695 |
| container_issue | 8 |
| container_start_page | 689 |
| container_title | Circulation research |
| container_volume | 91 |
| creator | Schulze, P Christian De Keulenaer, Gilles W Yoshioka, Jun Kassik, Kimberly A Lee, Richard T |
| description | ABSTRACT—Reactive oxygen species are important cellular signaling molecules, and thioredoxin (TRX) is a key regulator of cellular redox balance. We investigated the interaction of TRX with its endogenous inhibitor, vitamin D3–upregulated protein (VDUP)-1, in human aortic smooth muscle cells (SMCs). Adenoviral gene transfer of TRX enhanced TRX enzyme activity 2.7±0.4-fold (P |
| doi_str_mv | 10.1161/01.RES.0000037982.55074.F6 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_proquest_miscellaneous_72192963</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>72192963</sourcerecordid><originalsourceid>FETCH-LOGICAL-h2338-81a08c8424bf5a0b6fa2e30e9e4f1fb35fe884ed5bc9c26c80e62b44c3f62bab3</originalsourceid><addsrcrecordid>eNpFkd1u1DAQhS0EokvhFZCFBIILB_8lcS7RbguViqja3eUycpxJY3DixU5UuOMd2ifkSfC2i_DNWOd8c2TPIPSK0Yyxgr2nLLs8ucro_oiyUjzLc1rK7LR4hBYs55LIvGSP0SL5FSmFoEfoWYzfKGVS8OopOmJcqILJfIHutnbSgx3xSvz5fbvZBbienZ6gxRfBT2BHwvDb7WpzQdg7fHkwY7q1_idZwQ7GFsYJb3U0yQr4avB-6vHnORoHeAnO7YOc7SDoyfoRr_vg5-sen41Tksy99tWmlnVvfdjH2vE5etJpF-HFoR6jzenJevmJnH_5eLb8cE56LoQiimmqjJJcNl2uaVN0moOgUIHsWNeIvAOlJLR5YyrDC6MoFLyR0oguVd2IY_TmIXcX_I8Z4lQPNpr0Zj2Cn2NdclbxqhAJfHkA52aAtt4FO-jwq_43xwS8PgBpENp1QY_Gxv-cqCpWSpU4-cDdeJf-H7-7-QZC3YN2U1_fL5QyTjilnFGmKNlLSvwF69uWUQ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>72192963</pqid></control><display><type>article</type><title>Vitamin D3–Upregulated Protein-1 (VDUP-1) Regulates Redox-Dependent Vascular Smooth Muscle Cell Proliferation Through Interaction With Thioredoxin</title><source>Freely Accessible Journals</source><creator>Schulze, P Christian ; De Keulenaer, Gilles W ; Yoshioka, Jun ; Kassik, Kimberly A ; Lee, Richard T</creator><creatorcontrib>Schulze, P Christian ; De Keulenaer, Gilles W ; Yoshioka, Jun ; Kassik, Kimberly A ; Lee, Richard T</creatorcontrib><description><![CDATA[ABSTRACT—Reactive oxygen species are important cellular signaling molecules, and thioredoxin (TRX) is a key regulator of cellular redox balance. We investigated the interaction of TRX with its endogenous inhibitor, vitamin D3–upregulated protein (VDUP)-1, in human aortic smooth muscle cells (SMCs). Adenoviral gene transfer of TRX enhanced TRX enzyme activity 2.7±0.4-fold (P <0.05 versus cells infected with adenoviral vector expressing green fluorescent protein [AdGFP]) and resulted in a 3.8±0.5-fold increase of cellular DNA synthesis as detected by methyl-[H]thymidine incorporation (P <0.001). Platelet-derived growth factor (PDGF) also increased TRX enzyme activity 2.5±3.3-fold (P <0.05 versus no stimulation) and DNA synthesis 6.5±0.3-fold (P <0.001 versus no stimulation) without significant changes in TRX expression. PDGF and H2O2 time-dependently suppressed VDUP-1 expression (13-fold and 30-fold reduction after 1 hour, respectively;P <0.001), and this was inhibited by the cell-permeable antioxidants N-acetylcysteine and 4,5-dihydroxy-1,3-benzene-disulfonic acid (Tiron). Overexpression of VDUP-1 (AdVDUP-1) reduced TRX activity at baseline (−61±23% versus control cells, P <0.05) and abolished PDGF-induced TRX activity (−9±27% in AdVDUP-1–infected cells;P =NS versus control cells). In addition, overexpression of VDUP-1 blocked PDGF-induced DNA synthesis (1.3±0.4-fold increase in AdVDUP-1–infected cells versus 6.5±0.4-fold increase in AdGFP-infected cells, P <0.001). In conclusion, VDUP-1 has marked antiproliferative effects in SMCs through the suppression of TRX activity, suggesting that the regulation of VDUP-1 is a critical molecular switch in the transduction of pro-oxidant mitogenic signals. These data also demonstrate that activation of the reductase TRX plays a pivotal role in the redox-dependent proliferation of SMCs.]]></description><identifier>ISSN: 0009-7330</identifier><identifier>EISSN: 1524-4571</identifier><identifier>DOI: 10.1161/01.RES.0000037982.55074.F6</identifier><identifier>PMID: 12386145</identifier><identifier>CODEN: CIRUAL</identifier><language>eng</language><publisher>Hagerstown, MD: American Heart Association, Inc</publisher><subject>Active Transport, Cell Nucleus ; Adenoviridae - genetics ; Biological and medical sciences ; Blood vessels and receptors ; Carrier Proteins - genetics ; Carrier Proteins - physiology ; Cell Division ; Cell Nucleus - metabolism ; Cells, Cultured ; Fundamental and applied biological sciences. Psychology ; Genetic Vectors ; Humans ; Models, Biological ; Muscle, Smooth, Vascular - cytology ; Muscle, Smooth, Vascular - metabolism ; Oxidation-Reduction ; Oxidative Stress ; RNA, Messenger - biosynthesis ; Space life sciences ; Thioredoxins - genetics ; Thioredoxins - metabolism ; Transfection ; Vertebrates: cardiovascular system</subject><ispartof>Circulation research, 2002-10, Vol.91 (8), p.689-695</ispartof><rights>2002 American Heart Association, Inc.</rights><rights>2003 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13991748$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12386145$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Schulze, P Christian</creatorcontrib><creatorcontrib>De Keulenaer, Gilles W</creatorcontrib><creatorcontrib>Yoshioka, Jun</creatorcontrib><creatorcontrib>Kassik, Kimberly A</creatorcontrib><creatorcontrib>Lee, Richard T</creatorcontrib><title>Vitamin D3–Upregulated Protein-1 (VDUP-1) Regulates Redox-Dependent Vascular Smooth Muscle Cell Proliferation Through Interaction With Thioredoxin</title><title>Circulation research</title><addtitle>Circ Res</addtitle><description><![CDATA[ABSTRACT—Reactive oxygen species are important cellular signaling molecules, and thioredoxin (TRX) is a key regulator of cellular redox balance. We investigated the interaction of TRX with its endogenous inhibitor, vitamin D3–upregulated protein (VDUP)-1, in human aortic smooth muscle cells (SMCs). Adenoviral gene transfer of TRX enhanced TRX enzyme activity 2.7±0.4-fold (P <0.05 versus cells infected with adenoviral vector expressing green fluorescent protein [AdGFP]) and resulted in a 3.8±0.5-fold increase of cellular DNA synthesis as detected by methyl-[H]thymidine incorporation (P <0.001). Platelet-derived growth factor (PDGF) also increased TRX enzyme activity 2.5±3.3-fold (P <0.05 versus no stimulation) and DNA synthesis 6.5±0.3-fold (P <0.001 versus no stimulation) without significant changes in TRX expression. PDGF and H2O2 time-dependently suppressed VDUP-1 expression (13-fold and 30-fold reduction after 1 hour, respectively;P <0.001), and this was inhibited by the cell-permeable antioxidants N-acetylcysteine and 4,5-dihydroxy-1,3-benzene-disulfonic acid (Tiron). Overexpression of VDUP-1 (AdVDUP-1) reduced TRX activity at baseline (−61±23% versus control cells, P <0.05) and abolished PDGF-induced TRX activity (−9±27% in AdVDUP-1–infected cells;P =NS versus control cells). In addition, overexpression of VDUP-1 blocked PDGF-induced DNA synthesis (1.3±0.4-fold increase in AdVDUP-1–infected cells versus 6.5±0.4-fold increase in AdGFP-infected cells, P <0.001). In conclusion, VDUP-1 has marked antiproliferative effects in SMCs through the suppression of TRX activity, suggesting that the regulation of VDUP-1 is a critical molecular switch in the transduction of pro-oxidant mitogenic signals. These data also demonstrate that activation of the reductase TRX plays a pivotal role in the redox-dependent proliferation of SMCs.]]></description><subject>Active Transport, Cell Nucleus</subject><subject>Adenoviridae - genetics</subject><subject>Biological and medical sciences</subject><subject>Blood vessels and receptors</subject><subject>Carrier Proteins - genetics</subject><subject>Carrier Proteins - physiology</subject><subject>Cell Division</subject><subject>Cell Nucleus - metabolism</subject><subject>Cells, Cultured</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Genetic Vectors</subject><subject>Humans</subject><subject>Models, Biological</subject><subject>Muscle, Smooth, Vascular - cytology</subject><subject>Muscle, Smooth, Vascular - metabolism</subject><subject>Oxidation-Reduction</subject><subject>Oxidative Stress</subject><subject>RNA, Messenger - biosynthesis</subject><subject>Space life sciences</subject><subject>Thioredoxins - genetics</subject><subject>Thioredoxins - metabolism</subject><subject>Transfection</subject><subject>Vertebrates: cardiovascular system</subject><issn>0009-7330</issn><issn>1524-4571</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><recordid>eNpFkd1u1DAQhS0EokvhFZCFBIILB_8lcS7RbguViqja3eUycpxJY3DixU5UuOMd2ifkSfC2i_DNWOd8c2TPIPSK0Yyxgr2nLLs8ucro_oiyUjzLc1rK7LR4hBYs55LIvGSP0SL5FSmFoEfoWYzfKGVS8OopOmJcqILJfIHutnbSgx3xSvz5fbvZBbienZ6gxRfBT2BHwvDb7WpzQdg7fHkwY7q1_idZwQ7GFsYJb3U0yQr4avB-6vHnORoHeAnO7YOc7SDoyfoRr_vg5-sen41Tksy99tWmlnVvfdjH2vE5etJpF-HFoR6jzenJevmJnH_5eLb8cE56LoQiimmqjJJcNl2uaVN0moOgUIHsWNeIvAOlJLR5YyrDC6MoFLyR0oguVd2IY_TmIXcX_I8Z4lQPNpr0Zj2Cn2NdclbxqhAJfHkA52aAtt4FO-jwq_43xwS8PgBpENp1QY_Gxv-cqCpWSpU4-cDdeJf-H7-7-QZC3YN2U1_fL5QyTjilnFGmKNlLSvwF69uWUQ</recordid><startdate>20021018</startdate><enddate>20021018</enddate><creator>Schulze, P Christian</creator><creator>De Keulenaer, Gilles W</creator><creator>Yoshioka, Jun</creator><creator>Kassik, Kimberly A</creator><creator>Lee, Richard T</creator><general>American Heart Association, Inc</general><general>Lippincott</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>20021018</creationdate><title>Vitamin D3–Upregulated Protein-1 (VDUP-1) Regulates Redox-Dependent Vascular Smooth Muscle Cell Proliferation Through Interaction With Thioredoxin</title><author>Schulze, P Christian ; De Keulenaer, Gilles W ; Yoshioka, Jun ; Kassik, Kimberly A ; Lee, Richard T</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h2338-81a08c8424bf5a0b6fa2e30e9e4f1fb35fe884ed5bc9c26c80e62b44c3f62bab3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Active Transport, Cell Nucleus</topic><topic>Adenoviridae - genetics</topic><topic>Biological and medical sciences</topic><topic>Blood vessels and receptors</topic><topic>Carrier Proteins - genetics</topic><topic>Carrier Proteins - physiology</topic><topic>Cell Division</topic><topic>Cell Nucleus - metabolism</topic><topic>Cells, Cultured</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Genetic Vectors</topic><topic>Humans</topic><topic>Models, Biological</topic><topic>Muscle, Smooth, Vascular - cytology</topic><topic>Muscle, Smooth, Vascular - metabolism</topic><topic>Oxidation-Reduction</topic><topic>Oxidative Stress</topic><topic>RNA, Messenger - biosynthesis</topic><topic>Space life sciences</topic><topic>Thioredoxins - genetics</topic><topic>Thioredoxins - metabolism</topic><topic>Transfection</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Schulze, P Christian</creatorcontrib><creatorcontrib>De Keulenaer, Gilles W</creatorcontrib><creatorcontrib>Yoshioka, Jun</creatorcontrib><creatorcontrib>Kassik, Kimberly A</creatorcontrib><creatorcontrib>Lee, Richard T</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Schulze, P Christian</au><au>De Keulenaer, Gilles W</au><au>Yoshioka, Jun</au><au>Kassik, Kimberly A</au><au>Lee, Richard T</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Vitamin D3–Upregulated Protein-1 (VDUP-1) Regulates Redox-Dependent Vascular Smooth Muscle Cell Proliferation Through Interaction With Thioredoxin</atitle><jtitle>Circulation research</jtitle><addtitle>Circ Res</addtitle><date>2002-10-18</date><risdate>2002</risdate><volume>91</volume><issue>8</issue><spage>689</spage><epage>695</epage><pages>689-695</pages><issn>0009-7330</issn><eissn>1524-4571</eissn><coden>CIRUAL</coden><abstract><![CDATA[ABSTRACT—Reactive oxygen species are important cellular signaling molecules, and thioredoxin (TRX) is a key regulator of cellular redox balance. We investigated the interaction of TRX with its endogenous inhibitor, vitamin D3–upregulated protein (VDUP)-1, in human aortic smooth muscle cells (SMCs). Adenoviral gene transfer of TRX enhanced TRX enzyme activity 2.7±0.4-fold (P <0.05 versus cells infected with adenoviral vector expressing green fluorescent protein [AdGFP]) and resulted in a 3.8±0.5-fold increase of cellular DNA synthesis as detected by methyl-[H]thymidine incorporation (P <0.001). Platelet-derived growth factor (PDGF) also increased TRX enzyme activity 2.5±3.3-fold (P <0.05 versus no stimulation) and DNA synthesis 6.5±0.3-fold (P <0.001 versus no stimulation) without significant changes in TRX expression. PDGF and H2O2 time-dependently suppressed VDUP-1 expression (13-fold and 30-fold reduction after 1 hour, respectively;P <0.001), and this was inhibited by the cell-permeable antioxidants N-acetylcysteine and 4,5-dihydroxy-1,3-benzene-disulfonic acid (Tiron). Overexpression of VDUP-1 (AdVDUP-1) reduced TRX activity at baseline (−61±23% versus control cells, P <0.05) and abolished PDGF-induced TRX activity (−9±27% in AdVDUP-1–infected cells;P =NS versus control cells). In addition, overexpression of VDUP-1 blocked PDGF-induced DNA synthesis (1.3±0.4-fold increase in AdVDUP-1–infected cells versus 6.5±0.4-fold increase in AdGFP-infected cells, P <0.001). In conclusion, VDUP-1 has marked antiproliferative effects in SMCs through the suppression of TRX activity, suggesting that the regulation of VDUP-1 is a critical molecular switch in the transduction of pro-oxidant mitogenic signals. These data also demonstrate that activation of the reductase TRX plays a pivotal role in the redox-dependent proliferation of SMCs.]]></abstract><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>12386145</pmid><doi>10.1161/01.RES.0000037982.55074.F6</doi><tpages>7</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0009-7330 |
| ispartof | Circulation research, 2002-10, Vol.91 (8), p.689-695 |
| issn | 0009-7330 1524-4571 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_72192963 |
| source | Freely Accessible Journals |
| subjects | Active Transport, Cell Nucleus Adenoviridae - genetics Biological and medical sciences Blood vessels and receptors Carrier Proteins - genetics Carrier Proteins - physiology Cell Division Cell Nucleus - metabolism Cells, Cultured Fundamental and applied biological sciences. Psychology Genetic Vectors Humans Models, Biological Muscle, Smooth, Vascular - cytology Muscle, Smooth, Vascular - metabolism Oxidation-Reduction Oxidative Stress RNA, Messenger - biosynthesis Space life sciences Thioredoxins - genetics Thioredoxins - metabolism Transfection Vertebrates: cardiovascular system |
| title | Vitamin D3–Upregulated Protein-1 (VDUP-1) Regulates Redox-Dependent Vascular Smooth Muscle Cell Proliferation Through Interaction With Thioredoxin |
| url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-27T18%3A26%3A02IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Vitamin%20D3%E2%80%93Upregulated%20Protein-1%20(VDUP-1)%20Regulates%20Redox-Dependent%20Vascular%20Smooth%20Muscle%20Cell%20Proliferation%20Through%20Interaction%20With%20Thioredoxin&rft.jtitle=Circulation%20research&rft.au=Schulze,%20P%20Christian&rft.date=2002-10-18&rft.volume=91&rft.issue=8&rft.spage=689&rft.epage=695&rft.pages=689-695&rft.issn=0009-7330&rft.eissn=1524-4571&rft.coden=CIRUAL&rft_id=info:doi/10.1161/01.RES.0000037982.55074.F6&rft_dat=%3Cproquest_pubme%3E72192963%3C/proquest_pubme%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-h2338-81a08c8424bf5a0b6fa2e30e9e4f1fb35fe884ed5bc9c26c80e62b44c3f62bab3%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=72192963&rft_id=info:pmid/12386145&rfr_iscdi=true |