The Multiple Roles of EG-VEGF/PROK1 in Normal and Pathological Placental Angiogenesis
Identifieur interne : 000490 ( Pmc/Curation ); précédent : 000489; suivant : 000491The Multiple Roles of EG-VEGF/PROK1 in Normal and Pathological Placental Angiogenesis
Auteurs : Nadia Alfaidy [France] ; Pascale Hoffmann [France] ; Houssine Boufettal [Maroc] ; Naima Samouh [Maroc] ; Touria Aboussaouira [Maroc] ; Mohamed Benharouga [France] ; Jean-Jacques Feige [France] ; Sophie Brouillet [France]Source :
- BioMed Research International [ 2314-6133 ] ; 2014.
Abstract
Placentation is associated with several steps of vascular adaptations throughout pregnancy. These vascular changes occur both on the maternal and fetal sides, consisting of maternal uterine spiral arteries remodeling and placental vasculogenesis and angiogenesis, respectively. Placental angiogenesis is a pivotal process for efficient fetomaternal exchanges and placental development. This process is finely controlled throughout pregnancy, and it involves ubiquitous and pregnancy-specific angiogenic factors. In the last decade, endocrine gland derived vascular endothelial growth factor (EG-VEGF), also called prokineticin 1 (PROK1), has emerged as specific placental angiogenic factor that controls many aspects of normal and pathological placental angiogenesis such as recurrent pregnancy loss (RPL), gestational trophoblastic diseases (GTD), fetal growth restriction (FGR), and preeclampsia (PE). This review recapitulates EG-VEGF mediated-angiogenesis within the placenta and at the fetomaternal interface and proposes that its deregulation might contribute to the pathogenesis of several placental diseases including FGR and PE. More importantly this paper argues for EG-VEGF clinical relevance as a potential biomarker of the onset of pregnancy pathologies and discusses its potential usefulness for future therapeutic directions.
Url:
DOI: 10.1155/2014/451906
PubMed: 24955357
PubMed Central: 4052057
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">The Multiple Roles of EG-VEGF/PROK1 in Normal and Pathological Placental Angiogenesis</title>
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<author><name sortKey="Hoffmann, Pascale" sort="Hoffmann, Pascale" uniqKey="Hoffmann P" first="Pascale" last="Hoffmann">Pascale Hoffmann</name>
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<author><name sortKey="Boufettal, Houssine" sort="Boufettal, Houssine" uniqKey="Boufettal H" first="Houssine" last="Boufettal">Houssine Boufettal</name>
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<author><name sortKey="Benharouga, Mohamed" sort="Benharouga, Mohamed" uniqKey="Benharouga M" first="Mohamed" last="Benharouga">Mohamed Benharouga</name>
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<author><name sortKey="Feige, Jean Jacques" sort="Feige, Jean Jacques" uniqKey="Feige J" first="Jean-Jacques" last="Feige">Jean-Jacques Feige</name>
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<country xml:lang="fr">France</country>
<wicri:regionArea>Commissariat à l'Energie Atomique (CEA), DSV-iRTSV, 17 rue des Martyrs, 38054 Grenoble Cedex 9</wicri:regionArea>
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<wicri:regionArea>Université Grenoble-Alpes, 38041 Grenoble</wicri:regionArea>
</affiliation>
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<country xml:lang="fr">France</country>
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<author><name sortKey="Brouillet, Sophie" sort="Brouillet, Sophie" uniqKey="Brouillet S" first="Sophie" last="Brouillet">Sophie Brouillet</name>
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<country xml:lang="fr">France</country>
<wicri:regionArea>Commissariat à l'Energie Atomique (CEA), DSV-iRTSV, 17 rue des Martyrs, 38054 Grenoble Cedex 9</wicri:regionArea>
</affiliation>
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<wicri:regionArea>Université Grenoble-Alpes, 38041 Grenoble</wicri:regionArea>
</affiliation>
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<affiliation wicri:level="1"><nlm:aff id="I4">CHU de Grenoble, Hôpital Couple Enfant, Département de Génétique et Procréation, Centre d'Aide Médicale à la Procréation, CS 10217, 38043 Grenoble Cedex 9, France</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea>CHU de Grenoble, Hôpital Couple Enfant, Département de Génétique et Procréation, Centre d'Aide Médicale à la Procréation, CS 10217, 38043 Grenoble Cedex 9</wicri:regionArea>
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<series><title level="j">BioMed Research International</title>
<idno type="ISSN">2314-6133</idno>
<idno type="eISSN">2314-6141</idno>
<imprint><date when="2014">2014</date>
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<front><div type="abstract" xml:lang="en"><p>Placentation is associated with several steps of vascular adaptations throughout pregnancy. These vascular changes occur both on the maternal and fetal sides, consisting of maternal uterine spiral arteries remodeling and placental vasculogenesis and angiogenesis, respectively. Placental angiogenesis is a pivotal process for efficient fetomaternal exchanges and placental development. This process is finely controlled throughout pregnancy, and it involves ubiquitous and pregnancy-specific angiogenic factors. In the last decade, endocrine gland derived vascular endothelial growth factor (EG-VEGF), also called prokineticin 1 (PROK1), has emerged as specific placental angiogenic factor that controls many aspects of normal and pathological placental angiogenesis such as recurrent pregnancy loss (RPL), gestational trophoblastic diseases (GTD), fetal growth restriction (FGR), and preeclampsia (PE). This review recapitulates EG-VEGF mediated-angiogenesis within the placenta and at the fetomaternal interface and proposes that its deregulation might contribute to the pathogenesis of several placental diseases including FGR and PE. More importantly this paper argues for EG-VEGF clinical relevance as a potential biomarker of the onset of pregnancy pathologies and discusses its potential usefulness for future therapeutic directions.</p>
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</TEI>
<pmc article-type="review-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Biomed Res Int</journal-id>
<journal-id journal-id-type="iso-abbrev">Biomed Res Int</journal-id>
<journal-id journal-id-type="publisher-id">BMRI</journal-id>
<journal-title-group><journal-title>BioMed Research International</journal-title>
</journal-title-group>
<issn pub-type="ppub">2314-6133</issn>
<issn pub-type="epub">2314-6141</issn>
<publisher><publisher-name>Hindawi Publishing Corporation</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">24955357</article-id>
<article-id pub-id-type="pmc">4052057</article-id>
<article-id pub-id-type="doi">10.1155/2014/451906</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Review Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>The Multiple Roles of EG-VEGF/PROK1 in Normal and Pathological Placental Angiogenesis</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Alfaidy</surname>
<given-names>Nadia</given-names>
</name>
<xref ref-type="aff" rid="I1"><sup>1</sup>
</xref>
<xref ref-type="aff" rid="I2"><sup>2</sup>
</xref>
<xref ref-type="aff" rid="I3"><sup>3</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Hoffmann</surname>
<given-names>Pascale</given-names>
</name>
<xref ref-type="aff" rid="I1"><sup>1</sup>
</xref>
<xref ref-type="aff" rid="I2"><sup>2</sup>
</xref>
<xref ref-type="aff" rid="I3"><sup>3</sup>
</xref>
<xref ref-type="aff" rid="I4"><sup>4</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Boufettal</surname>
<given-names>Houssine</given-names>
</name>
<xref ref-type="aff" rid="I5"><sup>5</sup>
</xref>
<xref ref-type="aff" rid="I6"><sup>6</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Samouh</surname>
<given-names>Naima</given-names>
</name>
<xref ref-type="aff" rid="I5"><sup>5</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Aboussaouira</surname>
<given-names>Touria</given-names>
</name>
<xref ref-type="aff" rid="I6"><sup>6</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Benharouga</surname>
<given-names>Mohamed</given-names>
</name>
<xref ref-type="aff" rid="I1"><sup>1</sup>
</xref>
<xref ref-type="aff" rid="I2"><sup>2</sup>
</xref>
<xref ref-type="aff" rid="I7"><sup>7</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Feige</surname>
<given-names>Jean-Jacques</given-names>
</name>
<xref ref-type="aff" rid="I1"><sup>1</sup>
</xref>
<xref ref-type="aff" rid="I2"><sup>2</sup>
</xref>
<xref ref-type="aff" rid="I3"><sup>3</sup>
</xref>
</contrib>
<contrib contrib-type="author"><contrib-id contrib-id-type="orcid">http://orcid.org/0000-0003-3354-1551</contrib-id>
<name><surname>Brouillet</surname>
<given-names>Sophie</given-names>
</name>
<xref ref-type="aff" rid="I1"><sup>1</sup>
</xref>
<xref ref-type="aff" rid="I2"><sup>2</sup>
</xref>
<xref ref-type="aff" rid="I3"><sup>3</sup>
</xref>
<xref ref-type="aff" rid="I4"><sup>4</sup>
</xref>
<xref ref-type="corresp" rid="cor1">*</xref>
</contrib>
</contrib-group>
<aff id="I1"><sup>1</sup>
Commissariat à l'Energie Atomique (CEA), DSV-iRTSV, 17 rue des Martyrs, 38054 Grenoble Cedex 9, France</aff>
<aff id="I2"><sup>2</sup>
Université Grenoble-Alpes, 38041 Grenoble, France</aff>
<aff id="I3"><sup>3</sup>
Institut National de la Santé et de la Recherche Médicale U1036 (INSERM U1036), Biologie du Cancer et de l'Infection, Laboratoire BCI-iRTSV, CEA Grenoble, 17 rue des Martyrs, 38054 Grenoble Cedex 9, France</aff>
<aff id="I4"><sup>4</sup>
CHU de Grenoble, Hôpital Couple Enfant, Département de Génétique et Procréation, Centre d'Aide Médicale à la Procréation, CS 10217, 38043 Grenoble Cedex 9, France</aff>
<aff id="I5"><sup>5</sup>
Service de Gynécologie-Obstétrique “C”, Centre Hospitalier Universitaire Ibn Rochd, Faculté de Médecine et de Pharmacie, Université Hassan II, Ain Chok, 1 rue des Hôpitaux-ex Banaflous, 20360 Casablanca, Morocco</aff>
<aff id="I6"><sup>6</sup>
Plateau Commun de Recherche, Unité de Culture Cellulaire, Faculté de Médecine et de Pharmacie, 19 rue Tarek Bnou Ziad, 20360 Casablanca, Morocco</aff>
<aff id="I7"><sup>7</sup>
Centre National de la Recherche Scientifique, UMR 5249, 38054 Grenoble Cedex 9, France</aff>
<author-notes><corresp id="cor1">*Sophie Brouillet: <email>sophie_brouillet@yahoo.fr</email>
</corresp>
<fn fn-type="other"><p>Academic Editor: Padma Murthi</p>
</fn>
</author-notes>
<pub-date pub-type="ppub"><year>2014</year>
</pub-date>
<pub-date pub-type="epub"><day>15</day>
<month>5</month>
<year>2014</year>
</pub-date>
<volume>2014</volume>
<elocation-id>451906</elocation-id>
<history><date date-type="received"><day>6</day>
<month>2</month>
<year>2014</year>
</date>
<date date-type="rev-recd"><day>8</day>
<month>4</month>
<year>2014</year>
</date>
<date date-type="accepted"><day>14</day>
<month>4</month>
<year>2014</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2014 Nadia Alfaidy et al.</copyright-statement>
<copyright-year>2014</copyright-year>
<license license-type="open-access"><license-p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</license-p>
</license>
</permissions>
<abstract><p>Placentation is associated with several steps of vascular adaptations throughout pregnancy. These vascular changes occur both on the maternal and fetal sides, consisting of maternal uterine spiral arteries remodeling and placental vasculogenesis and angiogenesis, respectively. Placental angiogenesis is a pivotal process for efficient fetomaternal exchanges and placental development. This process is finely controlled throughout pregnancy, and it involves ubiquitous and pregnancy-specific angiogenic factors. In the last decade, endocrine gland derived vascular endothelial growth factor (EG-VEGF), also called prokineticin 1 (PROK1), has emerged as specific placental angiogenic factor that controls many aspects of normal and pathological placental angiogenesis such as recurrent pregnancy loss (RPL), gestational trophoblastic diseases (GTD), fetal growth restriction (FGR), and preeclampsia (PE). This review recapitulates EG-VEGF mediated-angiogenesis within the placenta and at the fetomaternal interface and proposes that its deregulation might contribute to the pathogenesis of several placental diseases including FGR and PE. More importantly this paper argues for EG-VEGF clinical relevance as a potential biomarker of the onset of pregnancy pathologies and discusses its potential usefulness for future therapeutic directions.</p>
</abstract>
</article-meta>
</front>
<floats-group><fig id="fig1" orientation="portrait" position="float"><label>Figure 1</label>
<caption><p>Proposed model of EG-VEGF-mediated effects on the fetomaternal angiogenesis during the first trimester of pregnancy. (a) and (b) represent cartoons of placental villi with EG-VEGF expression and actions on CT and EVT. (a) During the first trimester, EG-VEGF increases CT proliferation via PROKR1 activation and inhibits EVT invasion via PROKR2 activation. EG-VEGF/PROKR actions participate actively in trophoblastic shell and plugs constitution and contribute to the maintenance of physiological hypoxia during the first trimester of pregnancy. (b) At the end of the first trimester, EG-VEGF secretion declines. This contributes with other factors to EVT invasion and to the establishment of the fetomaternal circulation.</p>
</caption>
<graphic xlink:href="BMRI2014-451906.001"></graphic>
</fig>
<fig id="fig2" orientation="portrait" position="float"><label>Figure 2</label>
<caption><p>EG-VEGF is a new placental angiogenic factor. It controls placental growth via its multiple actions on endothelial cells within the chorionic villi.</p>
</caption>
<graphic xlink:href="BMRI2014-451906.002"></graphic>
</fig>
</floats-group>
</pmc>
</record>
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