Evidence map›Paper›PMID 21876171›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2011

Connective tissue growth factor acts within both endothelial cells and beta cells to promote proliferation of developing beta cells.

Michelle A Guney, Christine P Petersen, Andre Boustani, Matthew R Duncan, Uma Gunasekaran, Renuka Menon, Courtney Warfield, Gary R Grotendorst, Anna L Means, Aris N Economides and 1 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
5.3field-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

52 citing papers in PubMed, 69 citations in OpenAlex.

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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

11 authors at 5 institutions in 3 countries.

Michelle A GuneyDepartment of Molecular Physiology and Biophysics, Division of Diabetes, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Christine P Petersen
Andre Boustani
Matthew R Duncan
Uma Gunasekaran
Renuka Menon
Courtney Warfield
Gary R Grotendorst
Anna L Means
Aris N Economides
Maureen Gannon
Diabetes Australia · AULovelace Respiratory Research Institute · USInstitute of Molecular Biology and Biophysics · RURegeneron (United States) · USVanderbilt University Medical Center · US

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MATTHEW J TYSKA · 1995 to 2026
$172.8M
Vanderbilt Diabetes Research CenterP30DK020593 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI OWEN P MCGUINNESS · 2012 to 2026
$29.3M
TRANSGENIC MOUSE/ ES CELL SHARES RESOURCESP60DK020593 · NIDDK · VANDERBILT UNIVERSITY · PI MCGUINNESS, OWEN P · 1986 to 2011
$28.1M
MULTIDISCIPLINARY TRAINING IN MOLECULAR ENDOCRINOLOGYT32DK007563 · NIDDK · VANDERBILT UNIVERSITY · PI Richard M O'Brien · 1988 to 2026
$15.9M
NCI NIH HHS CA68485NCI NIH HHS P30 CA068485NIDDK NIH HHS 5 T 32 DK07563NIDDK NIH HHS DK20593NIDDK NIH HHS P30 DK020593NIDDK NIH HHS P60 DK020593
6 · The paper itself

Abstract

Type 1 and type 2 diabetes result from an absolute or relative reduction in functional β-cell mass. One approach to replacing lost β-cell mass is transplantation of cadaveric islets; however, this approach is limited by lack of adequate donor tissue. Therefore, there is much interest in identifying factors that enhance β-cell differentiation and proliferation in vivo or in vitro. Connective tissue growth factor (CTGF) is a secreted molecule expressed in endothelial cells, pancreatic ducts, and embryonic β cells that we previously showed is required for β-cell proliferation, differentiation, and islet morphogenesis during development. The current study investigated the tissue interactions by which CTGF promotes normal pancreatic islet development. We found that loss of CTGF from either endothelial cells or β cells results in decreased embryonic β-cell proliferation, making CTGF unique as an identified β cell-derived factor that regulates embryonic β-cell proliferation. Endothelial CTGF inactivation was associated with decreased islet vascularity, highlighting the proposed role of endothelial cells in β-cell proliferation. Furthermore, CTGF overexpression in β cells during embryogenesis using an inducible transgenic system increased islet mass at birth by promoting proliferation of immature β cells, in the absence of changes in islet vascularity. Together, these findings demonstrate that CTGF acts in an autocrine manner during pancreas development and suggest that CTGF has the potential to enhance expansion of immature β cells in directed differentiation or regeneration protocols.

Indexed as

AnimalsAutocrine CommunicationCell LineageCell ProliferationCell SizeConnective Tissue Growth FactorEmbryonic DevelopmentEndothelial CellsInsulin-Secreting CellsMiceModels, BiologicalMorphogenesisRatsConnective Tissue Growth Factor

Identifiers

PMID21876171
PMCPMC3174622
OpenAlexW2026664054

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.