Evidence map›Paper›PMID 31525223›Full record

ArticlePloS one2019

Increased proliferation and altered cell cycle regulation in pancreatic stem cells derived from patients with congenital hyperinsulinism.

Sophie G Kellaway, Karolina Mosinska, Zainaba Mohamed, Alexander Ryan, Stephen Richardson, Melanie Newbould, Indraneel Banerjee, Mark J Dunne, Karen E Cosgrove

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 36% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Review
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Sophie G KellawayFaculty of Biology Medicine and Health, School of Medicine, Division of Diabetes Endocrinology and Gastroenterology, University of Manchester, Manchester, United Kingdom.ORCID 0000-0002-4011-7460
Karolina MosinskaFaculty of Biology Medicine and Health, School of Medicine, Division of Diabetes Endocrinology and Gastroenterology, University of Manchester, Manchester, United Kingdom.
Zainaba MohamedDepartment of Paediatric Endocrinology, Royal Manchester Children's Hospital, Manchester, United Kingdom.
Alexander RyanFaculty of Biology Medicine and Health, School of Medicine, Division of Diabetes Endocrinology and Gastroenterology, University of Manchester, Manchester, United Kingdom.
Stephen RichardsonFaculty of Biology Medicine and Health, School of Medicine, Division of Diabetes Endocrinology and Gastroenterology, University of Manchester, Manchester, United Kingdom.ORCID 0000-0002-7637-4135
Melanie NewbouldDepartment of Paediatric Histopathology, Royal Manchester Children's Hospital, Manchester, United Kingdom.
Indraneel BanerjeeDepartment of Paediatric Endocrinology, Royal Manchester Children's Hospital, Manchester, United Kingdom.
Mark J DunneFaculty of Biology Medicine and Health, School of Medicine, Division of Diabetes Endocrinology and Gastroenterology, University of Manchester, Manchester, United Kingdom.
Karen E CosgroveFaculty of Biology Medicine and Health, School of Medicine, Division of Diabetes Endocrinology and Gastroenterology, University of Manchester, Manchester, United Kingdom.
University of Manchester · GBRoyal Manchester Children's Hospital · GB

Funding

National Centre for the Replacement, Refinement and Reduction of Animals in Research NC/K500306/1
6 · The paper itself

Abstract

Congenital hyperinsulinism (CHI) is characterised by inappropriate insulin secretion causing profound hypoglycaemia and brain damage if inadequately controlled. Pancreatic tissue isolated from patients with diffuse CHI shows abnormal proliferation rates, the mechanisms of which are not fully resolved. Understanding cell proliferation in CHI may lead to new therapeutic options, alongside opportunities to manipulate β-cell mass in patients with diabetes. We aimed to generate cell-lines from CHI pancreatic tissue to provide in vitro model systems for research. Three pancreatic mesenchymal stem cell-lines (CHIpMSC1-3) were derived from patients with CHI disease variants: focal, atypical and diffuse. All CHIpMSC lines demonstrated increased proliferation compared with control adult-derived pMSCs. Cell cycle alterations including increased CDK1 levels and decreased p27Kip1 nuclear localisation were observed in CHIpMSCs when compared to control pMSCs. In conclusion, CHIpMSCs are a useful in vitro model to further understand the cell cycle alterations leading to increased islet cell proliferation in CHI.

Identifiers

PMID31525223
PMCPMC6746350
OpenAlexW2971646772

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.