An EG-VEGF-Dependent Decrease in Homeobox Gene NKX3.1 Contributes to Cytotrophoblast Dysfunction: A Possible Mechanism in Human Fetal Growth Restriction
Idiopathic fetal growth restriction (FGR) is frequently associated with placental insufficiency. Previous reports have provided evidence that endocrine gland-derived vascular endothelial growth factor (EG-VEGF), a placental secreted protein, is expressed during the first trimester of pregnancy, cont...
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| Veröffentlicht in: | Molecular medicine (Cambridge, Mass.) Mass.), 2015-01, Vol.21 (1), p.645-656 |
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| creator | Murthi, Padma Brouillet, Sophie Pratt, Anita Borg, Anthony Kalionis, Bill Goffin, Frederic Tsatsaris, Vassilis Munaut, Carine Feige, Jean-Jacques Benharouga, Mohamed Fournier, Thierry Alfaidy, Nadia |
| description | Idiopathic fetal growth restriction (FGR) is frequently associated with placental insufficiency. Previous reports have provided evidence that endocrine gland-derived vascular endothelial growth factor (EG-VEGF), a placental secreted protein, is expressed during the first trimester of pregnancy, controls both trophoblast proliferation and invasion, and its increased expression is associated with human FGR. In this study, we hypothesize that EG-VEGF-dependent changes in placental homeobox gene expressions contribute to trophoblast dysfunction in idiopathic FGR. The changes in EG-VEGF-dependent homeobox gene expressions were determined using a homeobox gene cDNA array on placental explants of 8-12 wks gestation after stimulation with EG-VEGF
for 24 h. The homeobox gene array identified a greater-than-five-fold increase in
,
,
,
,
,
and
, while
showed a greater-than-two-fold decrease in mRNA expression compared with untreated controls. Homeobox gene
was selected as a candidate because it is a downstream target of EG-VEGF and its expression and functional roles are largely unknown in control and idiopathic FGR-affected placentae. Real-time PCR and immunoblotting showed a significant decrease in
mRNA and protein levels, respectively, in placentae from FGR compared with control pregnancies. Gene inactivation
using short-interference RNA specific for
demonstrated an increase in BeWo cell differentiation and a decrease in HTR-8/SVneo proliferation. We conclude that the decreased expression of homeobox gene
downstream of EG-VEGF may contribute to the trophoblast dysfunction associated with idiopathic FGR pregnancies. |
| doi_str_mv | 10.2119/molmed.2015.00071 |
| format | Article |
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for 24 h. The homeobox gene array identified a greater-than-five-fold increase in
,
,
,
,
,
and
, while
showed a greater-than-two-fold decrease in mRNA expression compared with untreated controls. Homeobox gene
was selected as a candidate because it is a downstream target of EG-VEGF and its expression and functional roles are largely unknown in control and idiopathic FGR-affected placentae. Real-time PCR and immunoblotting showed a significant decrease in
mRNA and protein levels, respectively, in placentae from FGR compared with control pregnancies. Gene inactivation
using short-interference RNA specific for
demonstrated an increase in BeWo cell differentiation and a decrease in HTR-8/SVneo proliferation. We conclude that the decreased expression of homeobox gene
downstream of EG-VEGF may contribute to the trophoblast dysfunction associated with idiopathic FGR pregnancies.</description><identifier>ISSN: 1076-1551</identifier><identifier>ISSN: 1528-3658</identifier><identifier>EISSN: 1528-3658</identifier><identifier>DOI: 10.2119/molmed.2015.00071</identifier><identifier>PMID: 26208047</identifier><language>eng</language><publisher>England: BioMed Central</publisher><subject>Achievement tests ; Amniotic fluid ; Biochemistry, Molecular Biology ; Birth weight ; Cesarean section ; Development Biology ; Diabetes ; Embryology and Organogenesis ; Ethics ; Fetuses ; Genomics ; Gestational age ; Human health and pathology ; Human health sciences ; Life Sciences ; Médecine de la reproduction (Gynécologie, andrologie, obstétrique) ; Patients ; Placenta ; Pregnancy ; Reproductive medicine (gynecology, andrology, obstetrics) ; Sciences de la santé humaine ; Transcription factors ; Ultrasonic imaging ; Vagina ; Vascular endothelial growth factor</subject><ispartof>Molecular medicine (Cambridge, Mass.), 2015-01, Vol.21 (1), p.645-656</ispartof><rights>2015. This work is licensed under http://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><rights>Copyright 2015, The Feinstein Institute for Medical Research 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c505t-b91a0491eae18ccee25c32e31072c1a03eeff634d3d029e052f43cfb88d2b6b03</citedby><cites>FETCH-LOGICAL-c505t-b91a0491eae18ccee25c32e31072c1a03eeff634d3d029e052f43cfb88d2b6b03</cites><orcidid>0000-0003-2535-5134 ; 0000-0002-0718-2447 ; 0000-0002-7515-339X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4749495/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4749495/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26208047$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-01259406$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Murthi, Padma</creatorcontrib><creatorcontrib>Brouillet, Sophie</creatorcontrib><creatorcontrib>Pratt, Anita</creatorcontrib><creatorcontrib>Borg, Anthony</creatorcontrib><creatorcontrib>Kalionis, Bill</creatorcontrib><creatorcontrib>Goffin, Frederic</creatorcontrib><creatorcontrib>Tsatsaris, Vassilis</creatorcontrib><creatorcontrib>Munaut, Carine</creatorcontrib><creatorcontrib>Feige, Jean-Jacques</creatorcontrib><creatorcontrib>Benharouga, Mohamed</creatorcontrib><creatorcontrib>Fournier, Thierry</creatorcontrib><creatorcontrib>Alfaidy, Nadia</creatorcontrib><title>An EG-VEGF-Dependent Decrease in Homeobox Gene NKX3.1 Contributes to Cytotrophoblast Dysfunction: A Possible Mechanism in Human Fetal Growth Restriction</title><title>Molecular medicine (Cambridge, Mass.)</title><addtitle>Mol Med</addtitle><description>Idiopathic fetal growth restriction (FGR) is frequently associated with placental insufficiency. Previous reports have provided evidence that endocrine gland-derived vascular endothelial growth factor (EG-VEGF), a placental secreted protein, is expressed during the first trimester of pregnancy, controls both trophoblast proliferation and invasion, and its increased expression is associated with human FGR. In this study, we hypothesize that EG-VEGF-dependent changes in placental homeobox gene expressions contribute to trophoblast dysfunction in idiopathic FGR. The changes in EG-VEGF-dependent homeobox gene expressions were determined using a homeobox gene cDNA array on placental explants of 8-12 wks gestation after stimulation with EG-VEGF
for 24 h. The homeobox gene array identified a greater-than-five-fold increase in
,
,
,
,
,
and
, while
showed a greater-than-two-fold decrease in mRNA expression compared with untreated controls. Homeobox gene
was selected as a candidate because it is a downstream target of EG-VEGF and its expression and functional roles are largely unknown in control and idiopathic FGR-affected placentae. Real-time PCR and immunoblotting showed a significant decrease in
mRNA and protein levels, respectively, in placentae from FGR compared with control pregnancies. Gene inactivation
using short-interference RNA specific for
demonstrated an increase in BeWo cell differentiation and a decrease in HTR-8/SVneo proliferation. We conclude that the decreased expression of homeobox gene
downstream of EG-VEGF may contribute to the trophoblast dysfunction associated with idiopathic FGR pregnancies.</description><subject>Achievement tests</subject><subject>Amniotic fluid</subject><subject>Biochemistry, Molecular Biology</subject><subject>Birth weight</subject><subject>Cesarean section</subject><subject>Development Biology</subject><subject>Diabetes</subject><subject>Embryology and Organogenesis</subject><subject>Ethics</subject><subject>Fetuses</subject><subject>Genomics</subject><subject>Gestational age</subject><subject>Human health and pathology</subject><subject>Human health sciences</subject><subject>Life Sciences</subject><subject>Médecine de la reproduction (Gynécologie, andrologie, obstétrique)</subject><subject>Patients</subject><subject>Placenta</subject><subject>Pregnancy</subject><subject>Reproductive medicine (gynecology, andrology, obstetrics)</subject><subject>Sciences de la santé humaine</subject><subject>Transcription factors</subject><subject>Ultrasonic imaging</subject><subject>Vagina</subject><subject>Vascular endothelial growth factor</subject><issn>1076-1551</issn><issn>1528-3658</issn><issn>1528-3658</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNpdUsmOEzEUbCEQs8AHcEGWuMChg9deOCBFmSyIsAgB4mbZzuvEo2472N0Z8id8Lk4yjGBOfvKrKr9Xrix7RvCIElK_7nzbwWpEMREjjHFJHmTnRNAqZ4WoHqYal0VOhCBn2UWM1xhTIrh4nJ3RguIK8_I8-z12aDrPv0_ns_wKtuBW4Hp0BSaAioCsQwvfgdf-F5qDA_Tx_Q82ImjiXR-sHnqIqPdosu99H_x243WrYuLvYzM401vv3qAx-uxjtLoF9AHMRjkbu6Pw0CmHZtCrFs2Dv-k36AvEJHvkPckeNaqN8PT2vMy-zaZfJ4t8-Wn-bjJe5kZg0ee6JgrzmoACUhkDQIVhFFhanZrUYgBNUzC-YitMa8CCNpyZRlfViupCY3aZvT3pbgedzDRp_aBauQ22U2EvvbLy_46zG7n2O8lLXvNaJAF2EmgtrEH6oK3c0SPxWA_tWiojNUhKi0qSGgtOEuvVibW599hivJSHO0yoqDkudgfsy9sRg_85JItkZ6OBtlUO_BAlqWhRcCoYS9AX96DXfgguGSip4GVBaEHKhCInlAnpZwI0dxMQLA_JkqdkyUOy5DFZifP8X5_uGH-jxP4AWD3LHA</recordid><startdate>20150101</startdate><enddate>20150101</enddate><creator>Murthi, Padma</creator><creator>Brouillet, Sophie</creator><creator>Pratt, Anita</creator><creator>Borg, Anthony</creator><creator>Kalionis, Bill</creator><creator>Goffin, Frederic</creator><creator>Tsatsaris, Vassilis</creator><creator>Munaut, Carine</creator><creator>Feige, Jean-Jacques</creator><creator>Benharouga, Mohamed</creator><creator>Fournier, Thierry</creator><creator>Alfaidy, Nadia</creator><general>BioMed Central</general><general>Feinstein Institute for Medical Research</general><general>North Shore Long Island Jewish Research Institute</general><general>The Feinstein Institute Press</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>1XC</scope><scope>Q33</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-2535-5134</orcidid><orcidid>https://orcid.org/0000-0002-0718-2447</orcidid><orcidid>https://orcid.org/0000-0002-7515-339X</orcidid></search><sort><creationdate>20150101</creationdate><title>An EG-VEGF-Dependent Decrease in Homeobox Gene NKX3.1 Contributes to Cytotrophoblast Dysfunction: A Possible Mechanism in Human Fetal Growth Restriction</title><author>Murthi, Padma ; Brouillet, Sophie ; Pratt, Anita ; Borg, Anthony ; Kalionis, Bill ; Goffin, Frederic ; Tsatsaris, Vassilis ; Munaut, Carine ; Feige, Jean-Jacques ; Benharouga, Mohamed ; Fournier, Thierry ; Alfaidy, Nadia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c505t-b91a0491eae18ccee25c32e31072c1a03eeff634d3d029e052f43cfb88d2b6b03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Achievement tests</topic><topic>Amniotic fluid</topic><topic>Biochemistry, Molecular Biology</topic><topic>Birth weight</topic><topic>Cesarean section</topic><topic>Development Biology</topic><topic>Diabetes</topic><topic>Embryology and Organogenesis</topic><topic>Ethics</topic><topic>Fetuses</topic><topic>Genomics</topic><topic>Gestational age</topic><topic>Human health and pathology</topic><topic>Human health sciences</topic><topic>Life Sciences</topic><topic>Médecine de la reproduction (Gynécologie, andrologie, obstétrique)</topic><topic>Patients</topic><topic>Placenta</topic><topic>Pregnancy</topic><topic>Reproductive medicine (gynecology, andrology, obstetrics)</topic><topic>Sciences de la santé humaine</topic><topic>Transcription factors</topic><topic>Ultrasonic imaging</topic><topic>Vagina</topic><topic>Vascular endothelial growth factor</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Murthi, Padma</creatorcontrib><creatorcontrib>Brouillet, Sophie</creatorcontrib><creatorcontrib>Pratt, Anita</creatorcontrib><creatorcontrib>Borg, Anthony</creatorcontrib><creatorcontrib>Kalionis, Bill</creatorcontrib><creatorcontrib>Goffin, Frederic</creatorcontrib><creatorcontrib>Tsatsaris, Vassilis</creatorcontrib><creatorcontrib>Munaut, Carine</creatorcontrib><creatorcontrib>Feige, Jean-Jacques</creatorcontrib><creatorcontrib>Benharouga, Mohamed</creatorcontrib><creatorcontrib>Fournier, Thierry</creatorcontrib><creatorcontrib>Alfaidy, Nadia</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</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>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</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>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><collection>Université de Liège - Open Repository and Bibliography (ORBI)</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular medicine (Cambridge, Mass.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Murthi, Padma</au><au>Brouillet, Sophie</au><au>Pratt, Anita</au><au>Borg, Anthony</au><au>Kalionis, Bill</au><au>Goffin, Frederic</au><au>Tsatsaris, Vassilis</au><au>Munaut, Carine</au><au>Feige, Jean-Jacques</au><au>Benharouga, Mohamed</au><au>Fournier, Thierry</au><au>Alfaidy, Nadia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>An EG-VEGF-Dependent Decrease in Homeobox Gene NKX3.1 Contributes to Cytotrophoblast Dysfunction: A Possible Mechanism in Human Fetal Growth Restriction</atitle><jtitle>Molecular medicine (Cambridge, Mass.)</jtitle><addtitle>Mol Med</addtitle><date>2015-01-01</date><risdate>2015</risdate><volume>21</volume><issue>1</issue><spage>645</spage><epage>656</epage><pages>645-656</pages><issn>1076-1551</issn><issn>1528-3658</issn><eissn>1528-3658</eissn><abstract>Idiopathic fetal growth restriction (FGR) is frequently associated with placental insufficiency. Previous reports have provided evidence that endocrine gland-derived vascular endothelial growth factor (EG-VEGF), a placental secreted protein, is expressed during the first trimester of pregnancy, controls both trophoblast proliferation and invasion, and its increased expression is associated with human FGR. In this study, we hypothesize that EG-VEGF-dependent changes in placental homeobox gene expressions contribute to trophoblast dysfunction in idiopathic FGR. The changes in EG-VEGF-dependent homeobox gene expressions were determined using a homeobox gene cDNA array on placental explants of 8-12 wks gestation after stimulation with EG-VEGF
for 24 h. The homeobox gene array identified a greater-than-five-fold increase in
,
,
,
,
,
and
, while
showed a greater-than-two-fold decrease in mRNA expression compared with untreated controls. Homeobox gene
was selected as a candidate because it is a downstream target of EG-VEGF and its expression and functional roles are largely unknown in control and idiopathic FGR-affected placentae. Real-time PCR and immunoblotting showed a significant decrease in
mRNA and protein levels, respectively, in placentae from FGR compared with control pregnancies. Gene inactivation
using short-interference RNA specific for
demonstrated an increase in BeWo cell differentiation and a decrease in HTR-8/SVneo proliferation. We conclude that the decreased expression of homeobox gene
downstream of EG-VEGF may contribute to the trophoblast dysfunction associated with idiopathic FGR pregnancies.</abstract><cop>England</cop><pub>BioMed Central</pub><pmid>26208047</pmid><doi>10.2119/molmed.2015.00071</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0003-2535-5134</orcidid><orcidid>https://orcid.org/0000-0002-0718-2447</orcidid><orcidid>https://orcid.org/0000-0002-7515-339X</orcidid><oa>free_for_read</oa></addata></record> |
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| source | DOAJ Directory of Open Access Journals; SpringerLink Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Springer Nature OA Free Journals |
| subjects | Achievement tests Amniotic fluid Biochemistry, Molecular Biology Birth weight Cesarean section Development Biology Diabetes Embryology and Organogenesis Ethics Fetuses Genomics Gestational age Human health and pathology Human health sciences Life Sciences Médecine de la reproduction (Gynécologie, andrologie, obstétrique) Patients Placenta Pregnancy Reproductive medicine (gynecology, andrology, obstetrics) Sciences de la santé humaine Transcription factors Ultrasonic imaging Vagina Vascular endothelial growth factor |
| title | An EG-VEGF-Dependent Decrease in Homeobox Gene NKX3.1 Contributes to Cytotrophoblast Dysfunction: A Possible Mechanism in Human Fetal Growth Restriction |
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