Evidence map›Paper›PMID 27891249›Full record

ArticleDiseases (Basel, Switzerland)2013

Protein Kinase C Epsilon Contributes to NADPH Oxidase Activation in a Pre-Eclampsia Lymphoblast Cell Model.

Toryn M Poolman, Paulene A Quinn, Leong Ng

Open access · goldAbstract read
In one paragraph

Article in Diseases (Basel, Switzerland), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact, top 93% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Identification of Myeloid Protein Kinase C Epsilon as a Novel Atheroprotective Gene.Arteriosclerosis, thrombosis, and vascular biology · 2025
    Article
  2. Review
  3. Article
  4. Article
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

3 authors at 1 institution in 1 country.

Toryn M PoolmanPharmacology and Therapeutics Group, Department of Cardiovascular Sciences, Leicester Royal Infirmary and NIHR Cardiovascular Biomedical Research Unit, Clinical Sciences Building, Leicester, LE2 7LX, UK.
Paulene A QuinnPharmacology and Therapeutics Group, Department of Cardiovascular Sciences, Leicester Royal Infirmary and NIHR Cardiovascular Biomedical Research Unit, Clinical Sciences Building, Leicester, LE2 7LX, UK.
Leong NgPharmacology and Therapeutics Group, Department of Cardiovascular Sciences, Leicester Royal Infirmary and NIHR Cardiovascular Biomedical Research Unit, Clinical Sciences Building, Leicester, LE2 7LX, UK.
Leicester Royal Infirmary · GB

Funding

British Heart Foundation PG/04/093/17615
6 · The paper itself

Abstract

Pre-eclampsia is a pregnancy-specific disorder characterised by hypertension and proteinuria, which in severe cases results in multi-system disturbances. The maternal syndrome is associated with a pro-inflammatory state, consisting of leukocyte activation, which is thought to contribute to the widespread endothelial dysfunction. We previously showed increased activation of NADPH oxidase in pre-eclampsia, in both neutrophils and B-lymphoblast cell lines (B-LCLs). In this study, the mechanism by which NADPH oxidase activity is increased in pre-eclampsia was further investigated. NADPH oxidase activity was found to be increased in phorbol-12-myristate-13-acetate (PMA) stimulated B-LCLs isolated from women with pre-eclampsia. This correlated with an increase in protein kinase C (PKC) substrate phosphorylation, p47-phox phosphorylation (a regulatory component of NADPH oxidase) and p47-phox directed-kinase activity. Using ion exchange and hydroxyapatite chromatography we identified a major peak of PMA regulated p47-phox kinase activity. Chromatography fractions were probed for PKC isoforms. We found the major peak of p47-phox kinase activity could not be separated from the elution profile of PKC epsilon. Using a peptide inhibitor of PKC epsilon, PMA-induced reactive oxygen species (ROS) production could be reduced to that of a normal B-LCL. These data suggest a pro-inflammatory role for PKC epsilon in the pathogenesis of pre-eclampsia.

Indexed as

free radicalshypertensionNADPH oxidasepre-eclampsiaprotein kinase C

Identifiers

PMID27891249
PMCPMC5123718
OpenAlexW1991222020

What OpenQuestion 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 OpenQuestion graph.