Evidence map›Paper›PMID 18696047›Full record

ArticleDiabetologia2008

Insulin protein and proliferation in ductal cells in the transplanted pancreas of patients with type 1 diabetes and recurrence of autoimmunity.

A Martin-Pagola, G Sisino, G Allende, J Dominguez-Bendala, R Gianani, H Reijonen, G T Nepom, C Ricordi, P Ruiz, J Sageshima and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Diabetologia, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
7.4field-weighted citation impact, top 3% 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

34 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Single-cell resolution analysis of the human pancreatic ductal progenitor cell niche.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  11. Article
  12. Review
  13. Pancreatic Progenitors: There and Back Again.Trends in endocrinology and metabolism: TEM · 2019
    Review
  14. Article
  15. Article
  16. Review
  17. Development of the endocrine pancreas and novel strategies for β-cell mass restoration and diabetes therapy.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2015
    Review
  18. Pancreas β cell regeneration and type 1 diabetes (Review).Experimental and therapeutic medicine · 2015
    Article
  19. Review
  20. Adult tissue sources for new β cells.Translational research : the journal of laboratory and clinical medicine · 2014
    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

13 authors at 3 institutions in 1 country.

A Martin-PagolaDiabetes Research Institute, Leonard Miller School of Medicine, University of Miami, 1450 NW 10th Avenue, Miami, FL 33136, USA.
G Sisino
G Allende
J Dominguez-Bendala
R Gianani
H Reijonen
G T Nepom
C Ricordi
P Ruiz
J Sageshima
G Ciancio
G W Burke
A Pugliese
University of Miami · USBenaroya Research InstituteUniversity of Colorado Health · US

Funding

Recurrence of T1D in Pancreas TransplantationR01DK070011 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI BURKE, GEORGE WILLIAM · 2005 to 2009
$1.5M
NIDDK NIH HHS R01 DK070011NIDDK NIH HHS R01 DK 070011-01A1
6 · The paper itself

Abstract

aim/hypothesisWe investigated whether beta cell neoformation occurs in the transplanted pancreas in patients with type 1 diabetes who had received a simultaneous pancreas-kidney transplant (SPK) and later developed recurrence of autoimmunity.

methodsWe examined pancreas transplant biopsies from nine SPK patients with or without recurrent autoimmunity or recurrent diabetes and from 16 non-diabetic organ donors. Tissues were analysed by immunohistochemistry and immunofluorescence.

resultsNumerous cytokeratin-19 (CK-19)(+) pancreatic ductal cells stained for insulin in six SPK recipients with recurrent autoimmunity, in five of whom diabetes requiring insulin therapy recurred. These cells also stained for the transcription factor pancreatic-duodenal homeobox-1 (Pdx-1), which is implicated in pancreatic development and beta cell differentiation. The number of insulin(+) ductal cells varied, being highest in the patient with the most severe beta cell loss and lowest in the normoglycaemic patient. In the patient with the most severe beta cell loss, we detected insulin(+)CK-19(+)Pdx-1(+) cells staining for the proliferation-related Ki-67 antigen (Ki-67), indicating proliferation. We were unable to detect Ki-67(+) beta cells within the islets in any SPK patient. Some insulin(+)CK-19(-) ductal cells contained chromogranin A, suggesting further endocrine differentiation. Insulin(+) cells were rarely noted in the pancreas transplant ducts in three SPK patients without islet autoimmunity and in six of 16 non-diabetic organ donors; these insulin(+) cells were never CK-19(+). CONCLUSIONS/

interpretationInsulin(+) pancreatic ductal cells, some apparently proliferating, were found in the transplanted pancreas with recurrent islet autoimmunity/diabetes. Replicating beta cells were not detected within islets. The observed changes may represent attempts at tissue remodelling and beta cell regeneration involving ductal cells in the human transplanted pancreas, possibly stimulated by hyperglycaemia and chronic inflammation.

Indexed as

Pancreas TransplantationAdultAutoimmunityCell ProliferationDiabetes Mellitus, Type 1FemaleFluorescent Antibody TechniqueHumansImmunohistochemistryInsulinKi-67 AntigenMaleMiddle AgedPancreasPancreatic DuctsInsulinKi-67 Antigen

Identifiers

PMID18696047
PMCPMC3019613
OpenAlexW2093707110

What OpenQuestion holds

Textmetadata
LicenceTDM
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.