Reduced expression of netrin-1 is associated with fetal growth restriction
The objective of this study was to investigate the expression of netrin-1 in placenta from patients with fetal growth restriction (FGR) and its effect on the viability and apoptosis of human placental microvascular endothelial cells. Thirty-three patients with FGR (including eighteen severe cases) a...
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| Veröffentlicht in: | Molecular and cellular biochemistry 2011-04, Vol.350 (1-2), p.81-87 |
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| creator | Qian-hua, Wang Shao-ping, Zhong Jian-wen, Zhu Yun, Yang Li, Zou |
| description | The objective of this study was to investigate the expression of netrin-1 in placenta from patients with fetal growth restriction (FGR) and its effect on the viability and apoptosis of human placental microvascular endothelial cells. Thirty-three patients with FGR (including eighteen severe cases) and twenty-four normal late pregnant women were investigated. The expression of netrin-1 in placental tissues was detected by employing immunohistochemistry, real-time PCR, and Western blotting. Human placental microvascular endothelial cells were isolated and, after treatment with netrin-1, examined for their viability and apoptosis by using MTT assay and flow cytometry. We demonstrated that the netrin-1 was present in placenta. Netrin-1 was significantly reduced in pregnant women with FGR as compared with the controls. Furthermore, netrin-1 enhanced the viability of human placental microvascular endothelial cells and inhibited their apoptosis. Netrin-1 may regulate the development of placental vessels and plays a key role in the pathogenesis of FGR. |
| doi_str_mv | 10.1007/s11010-010-0684-2 |
| format | Article |
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Thirty-three patients with FGR (including eighteen severe cases) and twenty-four normal late pregnant women were investigated. The expression of netrin-1 in placental tissues was detected by employing immunohistochemistry, real-time PCR, and Western blotting. Human placental microvascular endothelial cells were isolated and, after treatment with netrin-1, examined for their viability and apoptosis by using MTT assay and flow cytometry. We demonstrated that the netrin-1 was present in placenta. Netrin-1 was significantly reduced in pregnant women with FGR as compared with the controls. Furthermore, netrin-1 enhanced the viability of human placental microvascular endothelial cells and inhibited their apoptosis. Netrin-1 may regulate the development of placental vessels and plays a key role in the pathogenesis of FGR.</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/s11010-010-0684-2</identifier><identifier>PMID: 21193949</identifier><language>eng</language><publisher>Boston: Boston : Springer US</publisher><subject>Adult ; Apoptosis ; Biochemistry ; Biomedical and Life Sciences ; Cardiology ; Case-Control Studies ; Cell Culture Techniques ; Cells, Cultured ; Cellular biology ; Down-Regulation - genetics ; Embryology ; Endothelial Cells - metabolism ; Endothelial Cells - pathology ; Female ; Fetal growth restriction ; Fetal Growth Retardation - genetics ; Fetal Growth Retardation - metabolism ; Fetal Growth Retardation - pathology ; Fetuses ; Gene expression ; Gestational Age ; Growth ; Humans ; Immunohistochemistry ; Life Sciences ; Medical Biochemistry ; Nerve Growth Factors - genetics ; Nerve Growth Factors - metabolism ; Netrin-1 ; Oncology ; placenta ; Placenta - blood supply ; Placenta - metabolism ; Placenta - pathology ; Pregnancy ; Pregnant women ; Proteins ; Tumor Suppressor Proteins - genetics ; Tumor Suppressor Proteins - metabolism ; Young Adult</subject><ispartof>Molecular and cellular biochemistry, 2011-04, Vol.350 (1-2), p.81-87</ispartof><rights>Springer Science+Business Media, LLC. 2010</rights><rights>COPYRIGHT 2011 Springer</rights><rights>Springer Science+Business Media, LLC. 2011</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c461t-12982d8143503e5fdb0130064efa09f177e78f0c093a297dbc7f4df0bff087013</citedby><cites>FETCH-LOGICAL-c461t-12982d8143503e5fdb0130064efa09f177e78f0c093a297dbc7f4df0bff087013</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11010-010-0684-2$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11010-010-0684-2$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21193949$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Qian-hua, Wang</creatorcontrib><creatorcontrib>Shao-ping, Zhong</creatorcontrib><creatorcontrib>Jian-wen, Zhu</creatorcontrib><creatorcontrib>Yun, Yang</creatorcontrib><creatorcontrib>Li, Zou</creatorcontrib><title>Reduced expression of netrin-1 is associated with fetal growth restriction</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><addtitle>Mol Cell Biochem</addtitle><description>The objective of this study was to investigate the expression of netrin-1 in placenta from patients with fetal growth restriction (FGR) and its effect on the viability and apoptosis of human placental microvascular endothelial cells. Thirty-three patients with FGR (including eighteen severe cases) and twenty-four normal late pregnant women were investigated. The expression of netrin-1 in placental tissues was detected by employing immunohistochemistry, real-time PCR, and Western blotting. Human placental microvascular endothelial cells were isolated and, after treatment with netrin-1, examined for their viability and apoptosis by using MTT assay and flow cytometry. We demonstrated that the netrin-1 was present in placenta. Netrin-1 was significantly reduced in pregnant women with FGR as compared with the controls. Furthermore, netrin-1 enhanced the viability of human placental microvascular endothelial cells and inhibited their apoptosis. Netrin-1 may regulate the development of placental vessels and plays a key role in the pathogenesis of FGR.</description><subject>Adult</subject><subject>Apoptosis</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cardiology</subject><subject>Case-Control Studies</subject><subject>Cell Culture Techniques</subject><subject>Cells, Cultured</subject><subject>Cellular biology</subject><subject>Down-Regulation - genetics</subject><subject>Embryology</subject><subject>Endothelial Cells - metabolism</subject><subject>Endothelial Cells - pathology</subject><subject>Female</subject><subject>Fetal growth restriction</subject><subject>Fetal Growth Retardation - genetics</subject><subject>Fetal Growth Retardation - metabolism</subject><subject>Fetal Growth Retardation - pathology</subject><subject>Fetuses</subject><subject>Gene expression</subject><subject>Gestational Age</subject><subject>Growth</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Life Sciences</subject><subject>Medical Biochemistry</subject><subject>Nerve Growth Factors - genetics</subject><subject>Nerve Growth Factors - metabolism</subject><subject>Netrin-1</subject><subject>Oncology</subject><subject>placenta</subject><subject>Placenta - blood supply</subject><subject>Placenta - metabolism</subject><subject>Placenta - pathology</subject><subject>Pregnancy</subject><subject>Pregnant women</subject><subject>Proteins</subject><subject>Tumor Suppressor Proteins - genetics</subject><subject>Tumor Suppressor Proteins - metabolism</subject><subject>Young Adult</subject><issn>0300-8177</issn><issn>1573-4919</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</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>eNp9kU9v1DAQxS0EosvCB-ACERw4pczYyTo-VhV_VQkJ6NnyOuPFVTZe7ESFb89sU0AghKyRZfv3xs9-QjxGOEUA_bIgAkJ9U5uuqeUdscJWq7oxaO6KFSiAukOtT8SDUq6AQUC8L04kolGmMSvx_iP1s6e-om-HTKXENFYpVCNNOY41VrFUrpTko5sYuo7TlyrQ5IZql9M1L1jDpJ9Y91DcC24o9Oh2XovL168-n7-tLz68eXd-dlH7ZoNTjdJ0su-wUS0oakO_BWSfm4aCAxPYLekugAejnDS633odmj7ANgToNLNr8WLpe8jp68z3230snobBjZTmYrtWSwOaX7gWz_4ir9KcRzbH0Ma0UmHL0PMF2rmBbBxDmrLzx5b2TLWdMZ1mr2tx-g-KR0_76NNIIfL-HwJcBD6nUjIFe8hx7_J3i2CP6dklPXtTnJ6VrHly63fe7qn_pfgZFwNyAQofjTvKvx_0v65PF1FwybpdjsVefpLHT0fTKq2V-gHi_qr6</recordid><startdate>20110401</startdate><enddate>20110401</enddate><creator>Qian-hua, Wang</creator><creator>Shao-ping, Zhong</creator><creator>Jian-wen, Zhu</creator><creator>Yun, Yang</creator><creator>Li, Zou</creator><general>Boston : Springer US</general><general>Springer US</general><general>Springer</general><general>Springer Nature B.V</general><scope>FBQ</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>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</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>C1K</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>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20110401</creationdate><title>Reduced expression of netrin-1 is associated with fetal growth restriction</title><author>Qian-hua, Wang ; Shao-ping, Zhong ; Jian-wen, Zhu ; Yun, Yang ; Li, Zou</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c461t-12982d8143503e5fdb0130064efa09f177e78f0c093a297dbc7f4df0bff087013</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Adult</topic><topic>Apoptosis</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Cardiology</topic><topic>Case-Control Studies</topic><topic>Cell Culture Techniques</topic><topic>Cells, Cultured</topic><topic>Cellular biology</topic><topic>Down-Regulation - 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Academic</collection><jtitle>Molecular and cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Qian-hua, Wang</au><au>Shao-ping, Zhong</au><au>Jian-wen, Zhu</au><au>Yun, Yang</au><au>Li, Zou</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reduced expression of netrin-1 is associated with fetal growth restriction</atitle><jtitle>Molecular and cellular biochemistry</jtitle><stitle>Mol Cell Biochem</stitle><addtitle>Mol Cell Biochem</addtitle><date>2011-04-01</date><risdate>2011</risdate><volume>350</volume><issue>1-2</issue><spage>81</spage><epage>87</epage><pages>81-87</pages><issn>0300-8177</issn><eissn>1573-4919</eissn><abstract>The objective of this study was to investigate the expression of netrin-1 in placenta from patients with fetal growth restriction (FGR) and its effect on the viability and apoptosis of human placental microvascular endothelial cells. Thirty-three patients with FGR (including eighteen severe cases) and twenty-four normal late pregnant women were investigated. The expression of netrin-1 in placental tissues was detected by employing immunohistochemistry, real-time PCR, and Western blotting. Human placental microvascular endothelial cells were isolated and, after treatment with netrin-1, examined for their viability and apoptosis by using MTT assay and flow cytometry. We demonstrated that the netrin-1 was present in placenta. Netrin-1 was significantly reduced in pregnant women with FGR as compared with the controls. Furthermore, netrin-1 enhanced the viability of human placental microvascular endothelial cells and inhibited their apoptosis. Netrin-1 may regulate the development of placental vessels and plays a key role in the pathogenesis of FGR.</abstract><cop>Boston</cop><pub>Boston : Springer US</pub><pmid>21193949</pmid><doi>10.1007/s11010-010-0684-2</doi><tpages>7</tpages></addata></record> |
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| subjects | Adult Apoptosis Biochemistry Biomedical and Life Sciences Cardiology Case-Control Studies Cell Culture Techniques Cells, Cultured Cellular biology Down-Regulation - genetics Embryology Endothelial Cells - metabolism Endothelial Cells - pathology Female Fetal growth restriction Fetal Growth Retardation - genetics Fetal Growth Retardation - metabolism Fetal Growth Retardation - pathology Fetuses Gene expression Gestational Age Growth Humans Immunohistochemistry Life Sciences Medical Biochemistry Nerve Growth Factors - genetics Nerve Growth Factors - metabolism Netrin-1 Oncology placenta Placenta - blood supply Placenta - metabolism Placenta - pathology Pregnancy Pregnant women Proteins Tumor Suppressor Proteins - genetics Tumor Suppressor Proteins - metabolism Young Adult |
| title | Reduced expression of netrin-1 is associated with fetal growth restriction |
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