The effects of cadmium on VEGF-mediated angiogenesis in HUVECs
ABSTRACT Cadmium (Cd) is a highly toxic element that causes morphologic alterations and dysfunction in blood vessels. The altered vascular function caused by cadmium has been implicated in a range of chronic diseases, including hypertension. The effects of cadmium are a multisystem phenomenon involv...
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| Veröffentlicht in: | Journal of applied toxicology 2012-05, Vol.32 (5), p.342-349 |
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| creator | Kim, Jisun Lim, Wonbong Ko, Youngjong Kwon, HyukIl Kim, Sangwoo Kim, Oksu Park, Gyeongju Choi, Hongran Kim, Okjoon |
| description | ABSTRACT
Cadmium (Cd) is a highly toxic element that causes morphologic alterations and dysfunction in blood vessels. The altered vascular function caused by cadmium has been implicated in a range of chronic diseases, including hypertension. The effects of cadmium are a multisystem phenomenon involving inflammation, hypertrophy, apoptosis, angiogenesis and important processes involved in vascular remodeling systems. Vascular endothelial growth factor (VEGF) plays a major role in cell growth and angiogenesis under pathologic conditions. VEGF secretion is related to anti‐apoptosis protein expression and attenuates apoptosis in endothelial cells. This study examined the VEGF‐dependent mechanisms of angiogenesis and apoptosis in cadmium‐treated endothelial cells (HUVECs). The effects and mechanisms of cadmium in endothelial cells (HUVECs) were examined by exposing the cells to different doses of cadmium chloride (2.5–40 μ m). After the cadmium treatment, the angiogenesis and apoptosis mechanisms related to VEGF in cadmium‐treated HUVECs were examined. As a result, the low concentration of cadmium increased the tube formation in HUVECs. In addition, cadmium at concentrations of 5 and 10 μ m increased VEGF secretion and VEGFR2 activity, which suggest that cadmium affects the growth of blood vessels. All three MAPK pathways, namely ERK, JNK and p38, were activated by cadmium in HUVECs. However, high concentrations of cadmium caused cell damage, disrupted tube formation and inhibited VEGF expression and the activities of VEGFR2 and MAPK in HUVECs. Cadmium has dual functions through VEGF‐dependent mechanisms in a dose‐dependent manner. In this study, the dual effects of cadmium might alter angiogenesis and induce apoptosis through VEGF pathways in HUVECs. Copyright © 2011 John Wiley & Sons, Ltd.
This study examined the VEGF‐dependent mechanisms of angiogenesis and apoptosis in cadmium‐treated endothelial cells (HUVECs). As a result, the low concentration of cadmium increased the tube formation in HUVECs. In addition, cadmium at concentrations of 5 μ M and 10 μ M increased VEGF secretion and VEGFR2. However, high concentrations of cadmium caused cell damage, disrupted tube formation and inhibited VEGF expression and the activities of VEGFR2. Therefore, the dual effects of cadmium might alter angiogenesis and induce apoptosis through VEGF pathways in HUVECs. |
| doi_str_mv | 10.1002/jat.1677 |
| format | Article |
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Cadmium (Cd) is a highly toxic element that causes morphologic alterations and dysfunction in blood vessels. The altered vascular function caused by cadmium has been implicated in a range of chronic diseases, including hypertension. The effects of cadmium are a multisystem phenomenon involving inflammation, hypertrophy, apoptosis, angiogenesis and important processes involved in vascular remodeling systems. Vascular endothelial growth factor (VEGF) plays a major role in cell growth and angiogenesis under pathologic conditions. VEGF secretion is related to anti‐apoptosis protein expression and attenuates apoptosis in endothelial cells. This study examined the VEGF‐dependent mechanisms of angiogenesis and apoptosis in cadmium‐treated endothelial cells (HUVECs). The effects and mechanisms of cadmium in endothelial cells (HUVECs) were examined by exposing the cells to different doses of cadmium chloride (2.5–40 μ m). After the cadmium treatment, the angiogenesis and apoptosis mechanisms related to VEGF in cadmium‐treated HUVECs were examined. As a result, the low concentration of cadmium increased the tube formation in HUVECs. In addition, cadmium at concentrations of 5 and 10 μ m increased VEGF secretion and VEGFR2 activity, which suggest that cadmium affects the growth of blood vessels. All three MAPK pathways, namely ERK, JNK and p38, were activated by cadmium in HUVECs. However, high concentrations of cadmium caused cell damage, disrupted tube formation and inhibited VEGF expression and the activities of VEGFR2 and MAPK in HUVECs. Cadmium has dual functions through VEGF‐dependent mechanisms in a dose‐dependent manner. In this study, the dual effects of cadmium might alter angiogenesis and induce apoptosis through VEGF pathways in HUVECs. Copyright © 2011 John Wiley & Sons, Ltd.
This study examined the VEGF‐dependent mechanisms of angiogenesis and apoptosis in cadmium‐treated endothelial cells (HUVECs). As a result, the low concentration of cadmium increased the tube formation in HUVECs. In addition, cadmium at concentrations of 5 μ M and 10 μ M increased VEGF secretion and VEGFR2. However, high concentrations of cadmium caused cell damage, disrupted tube formation and inhibited VEGF expression and the activities of VEGFR2. Therefore, the dual effects of cadmium might alter angiogenesis and induce apoptosis through VEGF pathways in HUVECs.</description><identifier>ISSN: 0260-437X</identifier><identifier>EISSN: 1099-1263</identifier><identifier>DOI: 10.1002/jat.1677</identifier><identifier>PMID: 21425301</identifier><identifier>CODEN: JJATDK</identifier><language>eng</language><publisher>Chichester, UK: John Wiley & Sons, Ltd</publisher><subject>angiogenesis ; Apoptosis ; Apoptosis - drug effects ; Biological and medical sciences ; Cadmium ; Cadmium - pharmacology ; Cell Proliferation - drug effects ; Chemical and industrial products toxicology. Toxic occupational diseases ; Damage ; Endothelial cells ; Endothelial Cells - drug effects ; Endothelium, Vascular - cytology ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - metabolism ; Formations ; Human umbilical vein endothelial cells (HUVECs) ; Humans ; Medical sciences ; Metals and various inorganic compounds ; Mitogen-Activated Protein Kinases - metabolism ; Neovascularization, Pathologic - metabolism ; Pathways ; Secretions ; Toxicology ; Tubes ; Umbilical Veins ; Vascular Endothelial Growth Factor A - metabolism ; Vascular Endothelial Growth Factor A - pharmacology ; Vascular Endothelial Growth Factor Receptor-2 - metabolism ; VEGF (vascular endothelial growth factor)</subject><ispartof>Journal of applied toxicology, 2012-05, Vol.32 (5), p.342-349</ispartof><rights>Copyright © 2011 John Wiley & Sons, Ltd.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2012 John Wiley & Sons, Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5487-17f85ede2447b141c1ef7d844a7cb30ff3e36a7dca0c1916ffa50e319bfcc02f3</citedby><cites>FETCH-LOGICAL-c5487-17f85ede2447b141c1ef7d844a7cb30ff3e36a7dca0c1916ffa50e319bfcc02f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjat.1677$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjat.1677$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,778,782,1414,27911,27912,45561,45562</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25840371$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21425301$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, Jisun</creatorcontrib><creatorcontrib>Lim, Wonbong</creatorcontrib><creatorcontrib>Ko, Youngjong</creatorcontrib><creatorcontrib>Kwon, HyukIl</creatorcontrib><creatorcontrib>Kim, Sangwoo</creatorcontrib><creatorcontrib>Kim, Oksu</creatorcontrib><creatorcontrib>Park, Gyeongju</creatorcontrib><creatorcontrib>Choi, Hongran</creatorcontrib><creatorcontrib>Kim, Okjoon</creatorcontrib><title>The effects of cadmium on VEGF-mediated angiogenesis in HUVECs</title><title>Journal of applied toxicology</title><addtitle>J. Appl. Toxicol</addtitle><description>ABSTRACT
Cadmium (Cd) is a highly toxic element that causes morphologic alterations and dysfunction in blood vessels. The altered vascular function caused by cadmium has been implicated in a range of chronic diseases, including hypertension. The effects of cadmium are a multisystem phenomenon involving inflammation, hypertrophy, apoptosis, angiogenesis and important processes involved in vascular remodeling systems. Vascular endothelial growth factor (VEGF) plays a major role in cell growth and angiogenesis under pathologic conditions. VEGF secretion is related to anti‐apoptosis protein expression and attenuates apoptosis in endothelial cells. This study examined the VEGF‐dependent mechanisms of angiogenesis and apoptosis in cadmium‐treated endothelial cells (HUVECs). The effects and mechanisms of cadmium in endothelial cells (HUVECs) were examined by exposing the cells to different doses of cadmium chloride (2.5–40 μ m). After the cadmium treatment, the angiogenesis and apoptosis mechanisms related to VEGF in cadmium‐treated HUVECs were examined. As a result, the low concentration of cadmium increased the tube formation in HUVECs. In addition, cadmium at concentrations of 5 and 10 μ m increased VEGF secretion and VEGFR2 activity, which suggest that cadmium affects the growth of blood vessels. All three MAPK pathways, namely ERK, JNK and p38, were activated by cadmium in HUVECs. However, high concentrations of cadmium caused cell damage, disrupted tube formation and inhibited VEGF expression and the activities of VEGFR2 and MAPK in HUVECs. Cadmium has dual functions through VEGF‐dependent mechanisms in a dose‐dependent manner. In this study, the dual effects of cadmium might alter angiogenesis and induce apoptosis through VEGF pathways in HUVECs. Copyright © 2011 John Wiley & Sons, Ltd.
This study examined the VEGF‐dependent mechanisms of angiogenesis and apoptosis in cadmium‐treated endothelial cells (HUVECs). As a result, the low concentration of cadmium increased the tube formation in HUVECs. In addition, cadmium at concentrations of 5 μ M and 10 μ M increased VEGF secretion and VEGFR2. However, high concentrations of cadmium caused cell damage, disrupted tube formation and inhibited VEGF expression and the activities of VEGFR2. Therefore, the dual effects of cadmium might alter angiogenesis and induce apoptosis through VEGF pathways in HUVECs.</description><subject>angiogenesis</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Biological and medical sciences</subject><subject>Cadmium</subject><subject>Cadmium - pharmacology</subject><subject>Cell Proliferation - drug effects</subject><subject>Chemical and industrial products toxicology. Toxic occupational diseases</subject><subject>Damage</subject><subject>Endothelial cells</subject><subject>Endothelial Cells - drug effects</subject><subject>Endothelium, Vascular - cytology</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Formations</subject><subject>Human umbilical vein endothelial cells (HUVECs)</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Metals and various inorganic compounds</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>Neovascularization, Pathologic - metabolism</subject><subject>Pathways</subject><subject>Secretions</subject><subject>Toxicology</subject><subject>Tubes</subject><subject>Umbilical Veins</subject><subject>Vascular Endothelial Growth Factor A - metabolism</subject><subject>Vascular Endothelial Growth Factor A - pharmacology</subject><subject>Vascular Endothelial Growth Factor Receptor-2 - metabolism</subject><subject>VEGF (vascular endothelial growth factor)</subject><issn>0260-437X</issn><issn>1099-1263</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0E1rFEEQBuBGFLNGwV8gAyJ4mVjVH9OzFyEsm10lUZBN3FvT21Mde52POD2D5t_bS8YEBPFUh3p4i3oZe4lwggD83d4OJ1ho_YjNEObzHHkhHrMZ8AJyKfT2iD2LcQ-Qdrx8yo44Sq4E4Iy933yjjLwnN8Ss85mzVRPGJuva7Gq5OssbqoIdqMpsex26a2ophpiFNltfXi0X8Tl74m0d6cU0j9nl2XKzWOfnn1cfFqfnuVOy1DlqXyqqiEupdyjRIXldlVJa7XYCvBckCqsrZ8HhHAvvrQISON9554B7ccze3uXe9N2PkeJgmhAd1bVtqRujQa2EAs6V_j9VBSAXvMREX_9F993Yt-mRpKQCLXTBHwJd38XYkzc3fWhsf2sQzKF-k-o3h_oTfTUFjrvU3D3803cCbyZgo7O1723rQnxwqpQg9MHld-5nqOn2nwfNx9PNdHjyIQ70697b_rsp0hfKfP20Ml_g4mK7XSuzEL8BVDWnJg</recordid><startdate>201205</startdate><enddate>201205</enddate><creator>Kim, Jisun</creator><creator>Lim, Wonbong</creator><creator>Ko, Youngjong</creator><creator>Kwon, HyukIl</creator><creator>Kim, Sangwoo</creator><creator>Kim, Oksu</creator><creator>Park, Gyeongju</creator><creator>Choi, Hongran</creator><creator>Kim, Okjoon</creator><general>John Wiley & Sons, Ltd</general><general>Wiley</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><scope>IQODW</scope><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>7ST</scope><scope>7TK</scope><scope>7U7</scope><scope>C1K</scope><scope>K9.</scope><scope>SOI</scope><scope>8FD</scope><scope>FR3</scope><scope>KR7</scope></search><sort><creationdate>201205</creationdate><title>The effects of cadmium on VEGF-mediated angiogenesis in HUVECs</title><author>Kim, Jisun ; Lim, Wonbong ; Ko, Youngjong ; Kwon, HyukIl ; Kim, Sangwoo ; Kim, Oksu ; Park, Gyeongju ; Choi, Hongran ; Kim, Okjoon</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5487-17f85ede2447b141c1ef7d844a7cb30ff3e36a7dca0c1916ffa50e319bfcc02f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>angiogenesis</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Biological and medical sciences</topic><topic>Cadmium</topic><topic>Cadmium - pharmacology</topic><topic>Cell Proliferation - drug effects</topic><topic>Chemical and industrial products toxicology. Toxic occupational diseases</topic><topic>Damage</topic><topic>Endothelial cells</topic><topic>Endothelial Cells - drug effects</topic><topic>Endothelium, Vascular - cytology</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Formations</topic><topic>Human umbilical vein endothelial cells (HUVECs)</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Metals and various inorganic compounds</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>Neovascularization, Pathologic - metabolism</topic><topic>Pathways</topic><topic>Secretions</topic><topic>Toxicology</topic><topic>Tubes</topic><topic>Umbilical Veins</topic><topic>Vascular Endothelial Growth Factor A - metabolism</topic><topic>Vascular Endothelial Growth Factor A - pharmacology</topic><topic>Vascular Endothelial Growth Factor Receptor-2 - metabolism</topic><topic>VEGF (vascular endothelial growth factor)</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kim, Jisun</creatorcontrib><creatorcontrib>Lim, Wonbong</creatorcontrib><creatorcontrib>Ko, Youngjong</creatorcontrib><creatorcontrib>Kwon, HyukIl</creatorcontrib><creatorcontrib>Kim, Sangwoo</creatorcontrib><creatorcontrib>Kim, Oksu</creatorcontrib><creatorcontrib>Park, Gyeongju</creatorcontrib><creatorcontrib>Choi, Hongran</creatorcontrib><creatorcontrib>Kim, Okjoon</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Environment Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Environment Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Civil Engineering Abstracts</collection><jtitle>Journal of applied toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, Jisun</au><au>Lim, Wonbong</au><au>Ko, Youngjong</au><au>Kwon, HyukIl</au><au>Kim, Sangwoo</au><au>Kim, Oksu</au><au>Park, Gyeongju</au><au>Choi, Hongran</au><au>Kim, Okjoon</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The effects of cadmium on VEGF-mediated angiogenesis in HUVECs</atitle><jtitle>Journal of applied toxicology</jtitle><addtitle>J. Appl. Toxicol</addtitle><date>2012-05</date><risdate>2012</risdate><volume>32</volume><issue>5</issue><spage>342</spage><epage>349</epage><pages>342-349</pages><issn>0260-437X</issn><eissn>1099-1263</eissn><coden>JJATDK</coden><abstract>ABSTRACT
Cadmium (Cd) is a highly toxic element that causes morphologic alterations and dysfunction in blood vessels. The altered vascular function caused by cadmium has been implicated in a range of chronic diseases, including hypertension. The effects of cadmium are a multisystem phenomenon involving inflammation, hypertrophy, apoptosis, angiogenesis and important processes involved in vascular remodeling systems. Vascular endothelial growth factor (VEGF) plays a major role in cell growth and angiogenesis under pathologic conditions. VEGF secretion is related to anti‐apoptosis protein expression and attenuates apoptosis in endothelial cells. This study examined the VEGF‐dependent mechanisms of angiogenesis and apoptosis in cadmium‐treated endothelial cells (HUVECs). The effects and mechanisms of cadmium in endothelial cells (HUVECs) were examined by exposing the cells to different doses of cadmium chloride (2.5–40 μ m). After the cadmium treatment, the angiogenesis and apoptosis mechanisms related to VEGF in cadmium‐treated HUVECs were examined. As a result, the low concentration of cadmium increased the tube formation in HUVECs. In addition, cadmium at concentrations of 5 and 10 μ m increased VEGF secretion and VEGFR2 activity, which suggest that cadmium affects the growth of blood vessels. All three MAPK pathways, namely ERK, JNK and p38, were activated by cadmium in HUVECs. However, high concentrations of cadmium caused cell damage, disrupted tube formation and inhibited VEGF expression and the activities of VEGFR2 and MAPK in HUVECs. Cadmium has dual functions through VEGF‐dependent mechanisms in a dose‐dependent manner. In this study, the dual effects of cadmium might alter angiogenesis and induce apoptosis through VEGF pathways in HUVECs. Copyright © 2011 John Wiley & Sons, Ltd.
This study examined the VEGF‐dependent mechanisms of angiogenesis and apoptosis in cadmium‐treated endothelial cells (HUVECs). As a result, the low concentration of cadmium increased the tube formation in HUVECs. In addition, cadmium at concentrations of 5 μ M and 10 μ M increased VEGF secretion and VEGFR2. However, high concentrations of cadmium caused cell damage, disrupted tube formation and inhibited VEGF expression and the activities of VEGFR2. Therefore, the dual effects of cadmium might alter angiogenesis and induce apoptosis through VEGF pathways in HUVECs.</abstract><cop>Chichester, UK</cop><pub>John Wiley & Sons, Ltd</pub><pmid>21425301</pmid><doi>10.1002/jat.1677</doi><tpages>8</tpages></addata></record> |
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| subjects | angiogenesis Apoptosis Apoptosis - drug effects Biological and medical sciences Cadmium Cadmium - pharmacology Cell Proliferation - drug effects Chemical and industrial products toxicology. Toxic occupational diseases Damage Endothelial cells Endothelial Cells - drug effects Endothelium, Vascular - cytology Endothelium, Vascular - drug effects Endothelium, Vascular - metabolism Formations Human umbilical vein endothelial cells (HUVECs) Humans Medical sciences Metals and various inorganic compounds Mitogen-Activated Protein Kinases - metabolism Neovascularization, Pathologic - metabolism Pathways Secretions Toxicology Tubes Umbilical Veins Vascular Endothelial Growth Factor A - metabolism Vascular Endothelial Growth Factor A - pharmacology Vascular Endothelial Growth Factor Receptor-2 - metabolism VEGF (vascular endothelial growth factor) |
| title | The effects of cadmium on VEGF-mediated angiogenesis in HUVECs |
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