Vitamin D Prevents Endothelial Progenitor Cell Dysfunction Induced by Sera from Women with Preeclampsia or Conditioned Media from Hypoxic Placenta
Identifieur interne : 000849 ( Main/Exploration ); précédent : 000848; suivant : 000850Vitamin D Prevents Endothelial Progenitor Cell Dysfunction Induced by Sera from Women with Preeclampsia or Conditioned Media from Hypoxic Placenta
Auteurs : Lars Brodowski [Allemagne] ; Jennifer Burlakov [Allemagne] ; Ashley C. Myerski [États-Unis] ; Constantin S. Von Kaisenberg [Allemagne] ; Magdalena Grundmann [Allemagne] ; Carl A. Hubel [États-Unis] ; Frauke Von Versen-Höynck [Allemagne]Source :
- PLoS ONE [ 1932-6203 ] ; 2014.
Descripteurs français
- KwdFr :
- Adulte, Facteur de croissance endothéliale vasculaire de type A (antagonistes et inhibiteurs), Femelle, Grossesse, Humains, Hypoxie (anatomopathologie), Jeune adulte, Milieux de culture conditionnés, Placenta (anatomopathologie), Progéniteurs endothéliaux (), Progéniteurs endothéliaux (anatomopathologie), Prééclampsie (sang), Vitamine D (pharmacologie).
- MESH :
- anatomopathologie : Hypoxie, Placenta, Progéniteurs endothéliaux.
- antagonistes et inhibiteurs : Facteur de croissance endothéliale vasculaire de type A.
- pharmacologie : Vitamine D.
- sang : Prééclampsie.
- Adulte, Femelle, Grossesse, Humains, Jeune adulte, Milieux de culture conditionnés, Progéniteurs endothéliaux.
English descriptors
- KwdEn :
- Adult, Culture Media, Conditioned, Endothelial Progenitor Cells (drug effects), Endothelial Progenitor Cells (pathology), Female, Humans, Hypoxia (pathology), Placenta (pathology), Pre-Eclampsia (blood), Pregnancy, Vascular Endothelial Growth Factor A (antagonists & inhibitors), Vitamin D (pharmacology), Young Adult.
- MESH :
- chemical , antagonists & inhibitors : Vascular Endothelial Growth Factor A.
- chemical , pharmacology : Vitamin D.
- chemical : Culture Media, Conditioned.
- blood : Pre-Eclampsia.
- drug effects : Endothelial Progenitor Cells.
- pathology : Endothelial Progenitor Cells, Hypoxia, Placenta.
- Adult, Female, Humans, Pregnancy, Young Adult.
Abstract
Placenta-derived circulating factors contribute to the maternal endothelial dysfunction underlying preeclampsia. Endothelial colony forming cells (ECFC), a sub-population of endothelial progenitor cells (EPCs), are thought to be involved in vasculogenesis and endothelial repair. Low vitamin D concentrations are associated with an increased risk for preeclampsia.
We hypothesized that the function of human fetal ECFCs in culture would be suppressed by exposure to preeclampsia-related factors–preeclampsia serum or hypoxic placental conditioned medium– in a fashion reversed by vitamin D.
ECFCs were isolated from cord blood of uncomplicated pregnancies and expanded in culture. Uncomplicated pregnancy villous placenta in explant culture were exposed to either 2% (hypoxic), 8% (normoxic) or 21% (hyperoxic) O2 for 48 h, after which the conditioned media (CM) was collected.
ECFC tubule formation (Matrigel assay) and migration were examined in the presence of either maternal serum from preeclampsia cases or uncomplicated pregnancy controls, or pooled CM, in the presence or absence of 1,25(OH)2 vitamin D3.
1,25(OH)2 vitamin D3 reversed the adverse effects of preeclampsia serum or CM from hypoxic placenta on ECFCs capillary-tube formation and migration. Silencing of VDR expression by VDR siRNA, VDR blockade, or VEGF pathway blockade reduced ECFC functional abilities. Effects of VDR or VEGF blockade were partially prevented by vitamin D.
Vitamin D promotes the capillary-like tubule formation and migration of ECFCs in culture, minimizing the negative effects of exposure to preeclampsia-related factors. Further evaluation of the role of vitamin D in ECFC regulation and preeclampsia is warranted.
Url:
DOI: 10.1371/journal.pone.0098527
PubMed: 24887145
PubMed Central: 4041729
Affiliations:
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Le document en format XML
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<author><name sortKey="Von Kaisenberg, Constantin S" sort="Von Kaisenberg, Constantin S" uniqKey="Von Kaisenberg C" first="Constantin S." last="Von Kaisenberg">Constantin S. Von Kaisenberg</name>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term>
<term>Culture Media, Conditioned</term>
<term>Endothelial Progenitor Cells (drug effects)</term>
<term>Endothelial Progenitor Cells (pathology)</term>
<term>Female</term>
<term>Humans</term>
<term>Hypoxia (pathology)</term>
<term>Placenta (pathology)</term>
<term>Pre-Eclampsia (blood)</term>
<term>Pregnancy</term>
<term>Vascular Endothelial Growth Factor A (antagonists & inhibitors)</term>
<term>Vitamin D (pharmacology)</term>
<term>Young Adult</term>
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<keywords scheme="KwdFr" xml:lang="fr"><term>Adulte</term>
<term>Facteur de croissance endothéliale vasculaire de type A (antagonistes et inhibiteurs)</term>
<term>Femelle</term>
<term>Grossesse</term>
<term>Humains</term>
<term>Hypoxie (anatomopathologie)</term>
<term>Jeune adulte</term>
<term>Milieux de culture conditionnés</term>
<term>Placenta (anatomopathologie)</term>
<term>Progéniteurs endothéliaux ()</term>
<term>Progéniteurs endothéliaux (anatomopathologie)</term>
<term>Prééclampsie (sang)</term>
<term>Vitamine D (pharmacologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Vascular Endothelial Growth Factor A</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Vitamin D</term>
</keywords>
<keywords scheme="MESH" type="chemical" xml:lang="en"><term>Culture Media, Conditioned</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Hypoxie</term>
<term>Placenta</term>
<term>Progéniteurs endothéliaux</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Facteur de croissance endothéliale vasculaire de type A</term>
</keywords>
<keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>Pre-Eclampsia</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Endothelial Progenitor Cells</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Endothelial Progenitor Cells</term>
<term>Hypoxia</term>
<term>Placenta</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Vitamine D</term>
</keywords>
<keywords scheme="MESH" qualifier="sang" xml:lang="fr"><term>Prééclampsie</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Adult</term>
<term>Female</term>
<term>Humans</term>
<term>Pregnancy</term>
<term>Young Adult</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Adulte</term>
<term>Femelle</term>
<term>Grossesse</term>
<term>Humains</term>
<term>Jeune adulte</term>
<term>Milieux de culture conditionnés</term>
<term>Progéniteurs endothéliaux</term>
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<front><div type="abstract" xml:lang="en"><sec><title>Context</title>
<p>Placenta-derived circulating factors contribute to the maternal endothelial dysfunction underlying preeclampsia. Endothelial colony forming cells (ECFC), a sub-population of endothelial progenitor cells (EPCs), are thought to be involved in vasculogenesis and endothelial repair. Low vitamin D concentrations are associated with an increased risk for preeclampsia.</p>
</sec>
<sec><title>Objective</title>
<p>We hypothesized that the function of human fetal ECFCs in culture would be suppressed by exposure to preeclampsia-related factors–preeclampsia serum or hypoxic placental conditioned medium– in a fashion reversed by vitamin D.</p>
</sec>
<sec><title>Design, Setting, Patients</title>
<p>ECFCs were isolated from cord blood of uncomplicated pregnancies and expanded in culture. Uncomplicated pregnancy villous placenta in explant culture were exposed to either 2% (hypoxic), 8% (normoxic) or 21% (hyperoxic) O<sub>2</sub>
for 48 h, after which the conditioned media (CM) was collected.</p>
</sec>
<sec><title>Outcome Measures</title>
<p>ECFC tubule formation (Matrigel assay) and migration were examined in the presence of either maternal serum from preeclampsia cases or uncomplicated pregnancy controls, or pooled CM, in the presence or absence of 1,25(OH)<sub>2</sub>
vitamin D<sub>3</sub>
.</p>
</sec>
<sec><title>Results</title>
<p>1,25(OH)<sub>2</sub>
vitamin D<sub>3</sub>
reversed the adverse effects of preeclampsia serum or CM from hypoxic placenta on ECFCs capillary-tube formation and migration. Silencing of VDR expression by VDR siRNA, VDR blockade, or VEGF pathway blockade reduced ECFC functional abilities. Effects of VDR or VEGF blockade were partially prevented by vitamin D.</p>
</sec>
<sec><title>Conclusion</title>
<p>Vitamin D promotes the capillary-like tubule formation and migration of ECFCs in culture, minimizing the negative effects of exposure to preeclampsia-related factors. Further evaluation of the role of vitamin D in ECFC regulation and preeclampsia is warranted.</p>
</sec>
</div>
</front>
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