Placenta-Specific Genes, Their Regulation During Villous Trophoblast Differentiation and Dysregulation in Preterm Preeclampsia.
development
immune tolerance
metabolism
microarray
omics
transcriptional network
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
17 Jan 2020
17 Jan 2020
Historique:
received:
03
12
2019
revised:
07
01
2020
accepted:
08
01
2020
entrez:
23
1
2020
pubmed:
23
1
2020
medline:
24
10
2020
Statut:
epublish
Résumé
The human placenta maintains pregnancy and supports the developing fetus by providing nutrition, gas-waste exchange, hormonal regulation, and an immunological barrier from the maternal immune system. The villous syncytiotrophoblast carries most of these functions and provides the interface between the maternal and fetal circulatory systems. The syncytiotrophoblast is generated by the biochemical and morphological differentiation of underlying cytotrophoblast progenitor cells. The dysfunction of the villous trophoblast development is implicated in placenta-mediated pregnancy complications. Herein, we describe gene modules and clusters involved in the dynamic differentiation of villous cytotrophoblasts into the syncytiotrophoblast. During this process, the immune defense functions are first established, followed by structural and metabolic changes, and then by peptide hormone synthesis. We describe key transcription regulatory molecules that regulate gene modules involved in placental functions. Based on transcriptomic evidence, we infer how villous trophoblast differentiation and functions are dysregulated in preterm preeclampsia, a life-threatening placenta-mediated obstetrical syndrome for the mother and fetus. In the conclusion, we uncover the blueprint for villous trophoblast development and its impairment in preterm preeclampsia, which may aid in the future development of non-invasive biomarkers for placental functions and early identification of women at risk for preterm preeclampsia as well as other placenta-mediated pregnancy complications.
Identifiants
pubmed: 31963593
pii: ijms21020628
doi: 10.3390/ijms21020628
pmc: PMC7013556
pii:
doi:
Substances chimiques
Genetic Markers
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NICHD NIH HHS
ID : HHSN275201300006C
Pays : United States
Organisme : Magyar Tudományos Akadémia
ID : Momentum LP2014-7/2014
Organisme : MedInProt Protein Science Research Synergy Program
ID : Synergy IV and Adhoc Program
Organisme : Hungarian Scientific Research Fund
ID : K124862, K128262
Organisme : Nemzeti Kutatási, Fejlesztési és Innovaciós Alap
ID : FIEK_16-1-2016-0005
Organisme : Hungarian Ministry for National Economy
ID : VEKOP-2.3.3-15-2017-0014
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