Evidence map›Paper›PMID 23863477›Full record

ArticleDevelopment (Cambridge, England)2013

β1 integrin is a crucial regulator of pancreatic β-cell expansion.

Giuseppe R Diaferia, Antonio J Jimenez-Caliani, Prerana Ranjitkar, Wendy Yang, Gary Hardiman, Christopher J Rhodes, Laura Crisa, Vincenzo Cirulli

Abstract read
In one paragraph

Article in Development (Cambridge, England), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

48 citing papers in PubMed, 84 citations in OpenAlex.

  1. Observational
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Insulin secretion hot spots in pancreatic β cells as secreting adhesions.Frontiers in cell and developmental biology · 2023
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Collagen IV-β1-Integrin Influences INS-1 Cell Insulin SecretionFrontiers in cell and developmental biology · 2022
    Article
  16. Article
  17. Article
  18. Islet Regeneration: Endogenous and Exogenous Approaches.International journal of molecular sciences · 2021
    Review
  19. Article
  20. 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

8 authors at 2 institutions in 2 countries.

Giuseppe R DiaferiaDepartment of Experimental Oncology, European Institute of Oncology (IEO), Via Adamello 16 20139, Milan, Italy.
Antonio J Jimenez-Caliani
Prerana Ranjitkar
Wendy Yang
Gary Hardiman
Christopher J Rhodes
Laura Crisa
Vincenzo Cirulli
University of Washington · USEuropean Institute of Oncology · IT

Funding

Transgenic & Knock-out MouseP30DK063491 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI PETER J TONTONOZ · 2003 to 2026
$40.4M
Pharmacological Sciences SupplementT32GM007750 · NIGMS · UNIVERSITY OF WASHINGTON · PI ATKINS, WILLIAM M · 1985 to 2023
$12.6M
Diabetes, Obesity and Metabolism Training ProgramT32DK007247 · NIDDK · UNIVERSITY OF WASHINGTON · PI GREGORY J MORTON, KRISTINA Marie UTZSCHNEIDER · 1986 to 2026
$10.0M
METABOLIC CONTROL PROINSULIN BIOSYNTHESIS TRANSLATIONR01DK050610 · NIDDK · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI RHODES, CHRISTOPHER J · 1996 to 2014
$5.1M
MITOGENIC SIGNAL TRANSDUCTION IN PANCREATIC BETA CELLSR01DK055267 · NIDDK · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI RHODES, CHRISTOPHER J · 1998 to 2013
$4.3M
Endothelial Progenitors As Islet Vascular AddressR01HL075270 · NHLBI · UNIVERSITY OF WASHINGTON · PI CRISA, LAURA · 2006 to 2009
$1.7M
Howard Hughes Medical Institute 56006778NHLBI NIH HHS R01 HL075270NIDDK NIH HHS P30 DK063491NIDDK NIH HHS R01 DK050610NIDDK NIH HHS R01 DK055267NIDDK NIH HHS R01 DK55267NIDDK NIH HHS T32 DK007247NIGMS NIH HHS 5T32GM007750-34NIGMS NIH HHS T32 GM007750
6 · The paper itself

Abstract

Development of the endocrine compartment of the pancreas, as represented by the islets of Langerhans, occurs through a series of highly regulated events encompassing branching of the pancreatic epithelium, delamination and differentiation of islet progenitors from ductal domains, followed by expansion and three-dimensional organization into islet clusters. Cellular interactions with the extracellular matrix (ECM) mediated by receptors of the integrin family are postulated to regulate key functions in these processes. Yet, specific events regulated by these receptors in the developing pancreas remain unknown. Here, we show that ablation of the β1 integrin gene in developing pancreatic β-cells reduces their ability to expand during embryonic life, during the first week of postnatal life, and thereafter. Mice lacking β1 integrin in insulin-producing cells exhibit a dramatic reduction of the number of β-cells to only ∼18% of wild-type levels. Despite the significant reduction in β-cell mass, these mutant mice are not diabetic. A thorough phenotypic analysis of β-cells lacking β1 integrin revealed a normal expression repertoire of β-cell markers, normal architectural organization within islet clusters, and a normal ultrastructure. Global gene expression analysis revealed that ablation of this ECM receptor in β-cells inhibits the expression of genes regulating cell cycle progression. Collectively, our results demonstrate that β1 integrin receptors function as crucial positive regulators of β-cell expansion.

Indexed as

Cell ProliferationGene Expression Regulation, DevelopmentalAnimalsCell AdhesionCell CountCell CycleCell DifferentiationCell MembraneCells, CulturedCell ShapeEmbryo, MammalianExtracellular MatrixInsulinInsulin-Secreting CellsInsulin SecretionIntegrin beta1InsulinIntegrin beta1PTEN PhosphohydrolasePten protein, mouseCell adhesionExtracellular matrixIslets of LangerhansMouseProliferationβ1 integrinβ-cell development

Identifiers

PMID23863477
PMCPMC3737718
OpenAlexW2073934466

What OpenQuestion holds

Textmetadata
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.