Evidence map›Paper›PMID 28939845›Full record

ArticleScientific reports2017

FLT1 and transcriptome-wide polyadenylation site (PAS) analysis in preeclampsia.

Ami Ashar-Patel, Yasin Kaymaz, Augustine Rajakumar, Jeffrey A Bailey, S Ananth Karumanchi, Melissa J Moore

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
5.3field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 56 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Transforming Preeclampsia Care: Molecular Diagnostics and Therapeutic Innovations.Journal of the American Society of Nephrology : JASN · 2026
    Review
  4. Article
  5. Article
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  9. Review
  10. Placental Origins of Preeclampsia: Insights from Multi-Omic Studies.International journal of molecular sciences · 2024
    Review
  11. Article
  12. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Ami Ashar-PatelRNA Therapeutics Institute, University of Massachusetts Medical School, Worcester, MA, USA.
Yasin KaymazProgram in Bioinformatics and Integrative Biology, University of Massachusetts Medical School, Boston, MA, USA.ORCID 0000-0002-9725-7536
Augustine RajakumarDepartments of Gynecology and Obstetrics, Emory University, Atlanta, USA.ORCID 0000-0002-4975-6082
Jeffrey A BaileyProgram in Bioinformatics and Integrative Biology, University of Massachusetts Medical School, Boston, MA, USA.
S Ananth KarumanchiDepartments of Medicine, Obstetrics and Gynecology and Center for Vascular Biology Research, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA.
Melissa J MooreRNA Therapeutics Institute, University of Massachusetts Medical School, Worcester, MA, USA. melissa.moore@umassmed.edu.
University of Massachusetts Chan Medical School · USBeth Israel Deaconess Medical Center · US

Funding

Howard Hughes Medical Institute
6 · The paper itself

Abstract

Maternal symptoms of preeclampsia (PE) are primarily driven by excess anti-angiogenic factors originating from the placenta. Chief among these are soluble Flt1 proteins (sFlt1s) produced from alternatively polyadenylated mRNA isoforms. Here we used polyadenylation site sequencing (PAS-Seq) of RNA from normal and PE human placentae to interrogate transcriptome-wide gene expression and alternative polyadenylation signatures associated with early-onset PE (EO-PE; symptom onset < 34 weeks) and late-onset PE (LO-PE; symptom onset > 34 weeks) cohorts. While we observed no general shift in alternative polyadenylation associated with PE, the EO-PE and LO-PE cohorts do exhibit gene expression profiles distinct from both each other and from normal placentae. The only two genes upregulated across all transcriptome-wide PE analyses to date (microarray, RNA-Seq and PAS-Seq) are NRIP1 (RIP140), a transcriptional co-regulator linked to metabolic syndromes associated with obesity, and Flt1. Consistent with sFlt1 overproduction being a significant driver of clinical symptoms, placental Flt1 mRNA levels strongly correlate with maternal blood pressure. For Flt1, just three mRNA isoforms account for > 94% of all transcripts, with increased transcription of the entire locus driving Flt1 upregulation in both EO-PE and LO-PE. These three isoforms thus represent potential targets for therapeutic RNA interference (RNAi) in both early and late presentations.

Indexed as

PolyadenylationTranscriptomeAdultFemaleGene Expression ProfilingHumansPre-EclampsiaPregnancyRNA, MessengerVascular Endothelial Growth Factor Receptor-1Young AdultFLT1 protein, humanRNA, MessengerVascular Endothelial Growth Factor Receptor-1

Identifiers

PMID28939845
PMCPMC5610261
OpenAlexW2754446169

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.