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http://purl.uniprot.org/citations/34565269http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/34565269http://www.w3.org/2000/01/rdf-schema#comment"

Objective

Examine a mechanism of PLAC1 regulation and its potential role in preeclampsia (PE).

Materials and methods

Placental tissue samples and detailed clinical information were obtained through the University of Iowa Maternal Fetal Tissue Bank (IRB# 200910784) from gestational and maternal age-matched control (n = 17) and PE affected pregnancies (n = 12). PLAC1 and PLAC1 promoter-specific expression was measured using quantitative polymerase chain reaction (qPCR) and differences were assessed via the standard ΔΔCt method. In addition, the role of hypoxia in PLAC1 transcription was investigated through the exposure of HTR8/SVneo human trophoblast cells to the hypoxia mimic dimethyloxaloylglycine (DMOG).

Results

PLAC1 expression is seen to be 8.9-fold lower in human placentas affected by preeclampsia in comparison with controls (p < .05). Further, this decrease is paralleled by a significantly lower expression of the P2 or proximal PLAC1 promoter (p < .05). Expression of mediator complex subunit 1 (MED1), a known hypoxia-sensitive transcription coactivator and PLAC1 effector, is significantly correlated with PLAC 1 expression (r2 = 0.607, p < .001). These data suggest that PLAC1 expression is significantly down-regulated in preeclampsia at least in part via a MED1 hypoxia-mediated mechanism.

Conclusions

We confirm that PLAC1 transcription is suppressed in the placentae of women affected by preeclampsia. We further demonstrate that this suppression is driven through the P2 or proximal PLAC1 promoter. This demonstration led to the identification of the MED1-TRAP cofactor complex as the hypoxia-sensitive driver."xsd:string
http://purl.uniprot.org/citations/34565269http://purl.org/dc/terms/identifier"doi:10.1080/14767058.2021.1977792"xsd:string
http://purl.uniprot.org/citations/34565269http://purl.uniprot.org/core/author"Devor E.J."xsd:string
http://purl.uniprot.org/citations/34565269http://purl.uniprot.org/core/author"Warrier A."xsd:string
http://purl.uniprot.org/citations/34565269http://purl.uniprot.org/core/author"Santillan D.A."xsd:string
http://purl.uniprot.org/citations/34565269http://purl.uniprot.org/core/author"Scroggins S.M."xsd:string
http://purl.uniprot.org/citations/34565269http://purl.uniprot.org/core/author"Santillan M.K."xsd:string
http://purl.uniprot.org/citations/34565269http://purl.uniprot.org/core/date"2022"xsd:gYear
http://purl.uniprot.org/citations/34565269http://purl.uniprot.org/core/name"J Matern Fetal Neonatal Med"xsd:string
http://purl.uniprot.org/citations/34565269http://purl.uniprot.org/core/pages"8419-8425"xsd:string
http://purl.uniprot.org/citations/34565269http://purl.uniprot.org/core/title"Placenta-specific protein 1 (PLAC1) expression is significantly down-regulated in preeclampsia via a hypoxia-mediated mechanism."xsd:string
http://purl.uniprot.org/citations/34565269http://purl.uniprot.org/core/volume"35"xsd:string
http://purl.uniprot.org/citations/34565269http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/34565269
http://purl.uniprot.org/citations/34565269http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/34565269
http://purl.uniprot.org/uniprot/#_Q9HBJ0-mappedCitation-34565269http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/34565269
http://purl.uniprot.org/uniprot/Q9HBJ0http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/34565269