Vitamin D Antagonizes Negative Effects of Preeclampsia on Fetal Endothelial Colony Forming Cell Number and Function
Identifieur interne : 000852 ( Main/Exploration ); précédent : 000851; suivant : 000853Vitamin D Antagonizes Negative Effects of Preeclampsia on Fetal Endothelial Colony Forming Cell Number and Function
Auteurs : Frauke Von Versen-Höynck [Allemagne] ; Lars Brodowski [Allemagne] ; Ralf Dechend [Allemagne] ; Ashley C. Myerski [États-Unis] ; Carl A. Hubel [États-Unis]Source :
- PLoS ONE [ 1932-6203 ] ; 2014.
Descripteurs français
- KwdFr :
- Adulte, Calcitriol (pharmacologie), Cellules cultivées, Cellules endothéliales (cytologie), Cellules endothéliales (métabolisme), Facteur de croissance endothéliale vasculaire de type A (métabolisme), Femelle, Grossesse, Humains, Indoles (pharmacologie), Interférence par ARN, Microtubules (métabolisme), Mouvement cellulaire (), Petit ARN interférent (métabolisme), Prolifération cellulaire (), Prééclampsie (anatomopathologie), Prééclampsie (métabolisme), Pyrroles (pharmacologie), Récepteur calcitriol (antagonistes et inhibiteurs), Récepteur calcitriol (génétique), Récepteur calcitriol (métabolisme), Sang foetal (cytologie), Transduction du signal (), Études cas-témoins.
- MESH :
- anatomopathologie : Prééclampsie.
- antagonistes et inhibiteurs : Récepteur calcitriol.
- cytologie : Cellules endothéliales, Sang foetal.
- génétique : Récepteur calcitriol.
- métabolisme : Cellules endothéliales, Facteur de croissance endothéliale vasculaire de type A, Microtubules, Petit ARN interférent, Prééclampsie, Récepteur calcitriol.
- pharmacologie : Calcitriol, Indoles, Pyrroles.
- Adulte, Cellules cultivées, Femelle, Grossesse, Humains, Interférence par ARN, Mouvement cellulaire, Prolifération cellulaire, Transduction du signal, Études cas-témoins.
English descriptors
- KwdEn :
- Adult, Calcitriol (pharmacology), Case-Control Studies, Cell Movement (drug effects), Cell Proliferation (drug effects), Cells, Cultured, Endothelial Cells (cytology), Endothelial Cells (metabolism), Female, Fetal Blood (cytology), Humans, Indoles (pharmacology), Microtubules (metabolism), Pre-Eclampsia (metabolism), Pre-Eclampsia (pathology), Pregnancy, Pyrroles (pharmacology), RNA Interference, RNA, Small Interfering (metabolism), Receptors, Calcitriol (antagonists & inhibitors), Receptors, Calcitriol (genetics), Receptors, Calcitriol (metabolism), Signal Transduction (drug effects), Vascular Endothelial Growth Factor A (metabolism).
- MESH :
- chemical , antagonists & inhibitors : Receptors, Calcitriol.
- chemical , genetics : Receptors, Calcitriol.
- chemical , metabolism : RNA, Small Interfering, Receptors, Calcitriol, Vascular Endothelial Growth Factor A.
- chemical , pharmacology : Calcitriol, Indoles, Pyrroles.
- cytology : Endothelial Cells, Fetal Blood.
- drug effects : Cell Movement, Cell Proliferation, Signal Transduction.
- metabolism : Endothelial Cells, Microtubules, Pre-Eclampsia.
- pathology : Pre-Eclampsia.
- Adult, Case-Control Studies, Cells, Cultured, Female, Humans, Pregnancy, RNA Interference.
Abstract
Endothelial dysfunction is a primary feature of preeclampsia, a pregnancy complication associated with an increased future cardiovascular risk for mother and offspring. Endothelial colony forming cells (ECFC) are endothelial progenitor cells that participate in vasculogenesis and endothelial repair.
We hypothesized that the number and functional properties of fetal cord blood-derived ECFCs are reduced in preeclampsia compared to uncomplicated pregnancy (controls), and asked if adverse effects of preeclampsia on ECFC function are reversed by 1,25 (OH)2 vitamin D3.
This was a nested, case-control study. Forty women with uncomplicated pregnancy and 33 women with PE were recruited at Magee-Womens Hospital (USA) or at Hannover Medical School (Germany).
Time to ECFC colony appearance in culture, and number of colonies formed, were determined. Functional abilities of ECFCs were assessed
The number of cord ECFC colonies was lower (P = 0.04) in preeclampsia compared to controls. ECFCs from preeclampsia showed reduced proliferation (P<0.0001), formed fewer tubules (P = 0.02), and migrated less (P = 0.049) than control. Vitamin D3 significantly improved preeclampsia ECFC functional properties. VDR- or VEGF blockade reduced tubule formation, partially restorable by vitamin D3.
Fetal ECFCs from preeclamptic pregnancies are reduced in number and dysfunctional. Vitamin D3 had rescuing effects. This may have implications for the increased cardiovascular risk associated with preeclampsia.
Url:
DOI: 10.1371/journal.pone.0098990
PubMed: 24892558
PubMed Central: 4044051
Affiliations:
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Myerski</name><affiliation wicri:level="2"><nlm:aff id="aff3"><addr-line>Magee-Womens Research Institute and Department of Obstetrics, Gynecology & Reproductive Sciences, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Magee-Womens Research Institute and Department of Obstetrics, Gynecology & Reproductive Sciences, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania</wicri:regionArea><placeName><region type="state">Pennsylvanie</region></placeName></affiliation></author><author><name sortKey="Hubel, Carl A" sort="Hubel, Carl A" uniqKey="Hubel C" first="Carl A." last="Hubel">Carl A. Hubel</name><affiliation wicri:level="2"><nlm:aff id="aff3"><addr-line>Magee-Womens Research Institute and Department of Obstetrics, Gynecology & Reproductive Sciences, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Magee-Womens Research Institute and Department of Obstetrics, Gynecology & Reproductive Sciences, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania</wicri:regionArea><placeName><region type="state">Pennsylvanie</region></placeName></affiliation></author></analytic><series><title level="j">PLoS ONE</title><idno type="eISSN">1932-6203</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Calcitriol (pharmacology)</term><term>Case-Control Studies</term><term>Cell Movement (drug effects)</term><term>Cell Proliferation (drug effects)</term><term>Cells, Cultured</term><term>Endothelial Cells (cytology)</term><term>Endothelial Cells (metabolism)</term><term>Female</term><term>Fetal Blood (cytology)</term><term>Humans</term><term>Indoles (pharmacology)</term><term>Microtubules (metabolism)</term><term>Pre-Eclampsia (metabolism)</term><term>Pre-Eclampsia (pathology)</term><term>Pregnancy</term><term>Pyrroles (pharmacology)</term><term>RNA Interference</term><term>RNA, Small Interfering (metabolism)</term><term>Receptors, Calcitriol (antagonists & inhibitors)</term><term>Receptors, Calcitriol (genetics)</term><term>Receptors, Calcitriol (metabolism)</term><term>Signal Transduction (drug effects)</term><term>Vascular Endothelial Growth Factor A (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adulte</term><term>Calcitriol (pharmacologie)</term><term>Cellules cultivées</term><term>Cellules endothéliales (cytologie)</term><term>Cellules endothéliales (métabolisme)</term><term>Facteur de croissance endothéliale vasculaire de type A (métabolisme)</term><term>Femelle</term><term>Grossesse</term><term>Humains</term><term>Indoles (pharmacologie)</term><term>Interférence par ARN</term><term>Microtubules (métabolisme)</term><term>Mouvement cellulaire ()</term><term>Petit ARN interférent (métabolisme)</term><term>Prolifération cellulaire ()</term><term>Prééclampsie (anatomopathologie)</term><term>Prééclampsie (métabolisme)</term><term>Pyrroles (pharmacologie)</term><term>Récepteur calcitriol (antagonistes et inhibiteurs)</term><term>Récepteur calcitriol (génétique)</term><term>Récepteur calcitriol (métabolisme)</term><term>Sang foetal (cytologie)</term><term>Transduction du signal ()</term><term>Études cas-témoins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Receptors, Calcitriol</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Receptors, Calcitriol</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>RNA, Small Interfering</term><term>Receptors, Calcitriol</term><term>Vascular Endothelial Growth Factor A</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Calcitriol</term><term>Indoles</term><term>Pyrroles</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Prééclampsie</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Récepteur calcitriol</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Cellules endothéliales</term><term>Sang foetal</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Endothelial Cells</term><term>Fetal Blood</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Movement</term><term>Cell Proliferation</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Récepteur calcitriol</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Endothelial Cells</term><term>Microtubules</term><term>Pre-Eclampsia</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cellules endothéliales</term><term>Facteur de croissance endothéliale vasculaire de type A</term><term>Microtubules</term><term>Petit ARN interférent</term><term>Prééclampsie</term><term>Récepteur calcitriol</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Pre-Eclampsia</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Calcitriol</term><term>Indoles</term><term>Pyrroles</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Case-Control Studies</term><term>Cells, Cultured</term><term>Female</term><term>Humans</term><term>Pregnancy</term><term>RNA Interference</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Adulte</term><term>Cellules cultivées</term><term>Femelle</term><term>Grossesse</term><term>Humains</term><term>Interférence par ARN</term><term>Mouvement cellulaire</term><term>Prolifération cellulaire</term><term>Transduction du signal</term><term>Études cas-témoins</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec><title>Context</title><p>Endothelial dysfunction is a primary feature of preeclampsia, a pregnancy complication associated with an increased future cardiovascular risk for mother and offspring. Endothelial colony forming cells (ECFC) are endothelial progenitor cells that participate in vasculogenesis and endothelial repair.</p></sec><sec><title>Objective</title><p>We hypothesized that the number and functional properties of fetal cord blood-derived ECFCs are reduced in preeclampsia compared to uncomplicated pregnancy (controls), and asked if adverse effects of preeclampsia on ECFC function are reversed by 1,25 (OH)<sub>2</sub> vitamin D<sub>3</sub>.</p></sec><sec><title>Design, Setting, Patients</title><p>This was a nested, case-control study. Forty women with uncomplicated pregnancy and 33 women with PE were recruited at Magee-Womens Hospital (USA) or at Hannover Medical School (Germany).</p></sec><sec><title>Main Outcome Measures</title><p>Time to ECFC colony appearance in culture, and number of colonies formed, were determined. Functional abilities of ECFCs were assessed <italic>in vitro</italic> by tubule formation in Matrigel assay, migration, and proliferation. ECFC function was tested in the presence or absence of 1,25 (OH)<sub>2</sub> vitamin D<sub>3</sub>, and after vitamin D receptor (VDR) or VEGF signaling blockade.</p></sec><sec><title>Results</title><p>The number of cord ECFC colonies was lower (P = 0.04) in preeclampsia compared to controls. ECFCs from preeclampsia showed reduced proliferation (P<0.0001), formed fewer tubules (P = 0.02), and migrated less (P = 0.049) than control. Vitamin D<sub>3</sub> significantly improved preeclampsia ECFC functional properties. VDR- or VEGF blockade reduced tubule formation, partially restorable by vitamin D<sub>3</sub>.</p></sec><sec><title>Conclusion</title><p>Fetal ECFCs from preeclamptic pregnancies are reduced in number and dysfunctional. Vitamin D<sub>3</sub> had rescuing effects. This may have implications for the increased cardiovascular risk associated with preeclampsia.</p></sec></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Wang, Y" uniqKey="Wang Y">Y Wang</name></author><author><name sortKey="Gu, Y" uniqKey="Gu Y">Y Gu</name></author><author><name sortKey="Zhang, Y" uniqKey="Zhang Y">Y Zhang</name></author><author><name sortKey="Lewis, Df" uniqKey="Lewis D">DF Lewis</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Roberts, Jm" uniqKey="Roberts J">JM Roberts</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Roberts, Jm" uniqKey="Roberts J">JM Roberts</name></author><author><name sortKey="Bell, Mj" uniqKey="Bell M">MJ Bell</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Brown, Mc" uniqKey="Brown M">MC Brown</name></author><author><name sortKey="Best, Ke" uniqKey="Best K">KE 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Sipos</name></author><author><name sortKey="Bourque, Sl" uniqKey="Bourque S">SL Bourque</name></author><author><name sortKey="Hubel, Ca" uniqKey="Hubel C">CA Hubel</name></author><author><name sortKey="Baker, Pn" uniqKey="Baker P">PN Baker</name></author><author><name sortKey="Sibley, Cp" uniqKey="Sibley C">CP Sibley</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hwang, Hs" uniqKey="Hwang H">HS Hwang</name></author><author><name sortKey="Kwon, Yg" uniqKey="Kwon Y">YG Kwon</name></author><author><name sortKey="Kwon, Jy" uniqKey="Kwon J">JY Kwon</name></author><author><name sortKey="Won Park, Y" uniqKey="Won Park Y">Y Won Park</name></author><author><name sortKey="Maeng, Ys" uniqKey="Maeng Y">YS Maeng</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kajantie, E" uniqKey="Kajantie E">E Kajantie</name></author><author><name sortKey="Eriksson, Jg" uniqKey="Eriksson J">JG Eriksson</name></author><author><name sortKey="Osmond, C" uniqKey="Osmond C">C Osmond</name></author><author><name sortKey="Thornburg, K" uniqKey="Thornburg K">K Thornburg</name></author><author><name sortKey="Barker, Dj" uniqKey="Barker D">DJ Barker</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Davis, Ef" uniqKey="Davis E">EF Davis</name></author><author><name sortKey="Lazdam, M" uniqKey="Lazdam M">M Lazdam</name></author><author><name sortKey="Lewandowski, Aj" uniqKey="Lewandowski A">AJ Lewandowski</name></author><author><name sortKey="Worton, Sa" uniqKey="Worton S">SA Worton</name></author><author><name sortKey="Kelly, B" uniqKey="Kelly B">B Kelly</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>Allemagne</li><li>États-Unis</li></country><region><li>Basse-Saxe</li><li>Berlin</li><li>Pennsylvanie</li></region><settlement><li>Berlin</li><li>Hanovre</li></settlement></list><tree><country name="Allemagne"><region name="Basse-Saxe"><name sortKey="Von Versen Hoynck, Frauke" sort="Von Versen Hoynck, Frauke" uniqKey="Von Versen Hoynck F" first="Frauke" last="Von Versen-Höynck">Frauke Von Versen-Höynck</name></region><name sortKey="Brodowski, Lars" sort="Brodowski, Lars" uniqKey="Brodowski L" first="Lars" last="Brodowski">Lars Brodowski</name><name sortKey="Dechend, Ralf" sort="Dechend, Ralf" uniqKey="Dechend R" first="Ralf" last="Dechend">Ralf Dechend</name></country><country name="États-Unis"><region name="Pennsylvanie"><name sortKey="Myerski, Ashley C" sort="Myerski, Ashley C" uniqKey="Myerski A" first="Ashley C." last="Myerski">Ashley C. 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