Evidence map›Paper›PMID 26398949›Full record

ArticleDisease models & mechanisms2015

Human umbilical cord matrix-derived stem cells exert trophic effects on β-cell survival in diabetic rats and isolated islets.

Yunting Zhou, Qi Hu, Fuyi Chen, Juan Zhang, Jincheng Guo, Hongwu Wang, Jiang Gu, Lian Ma, Guyu Ho

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Disease models & mechanisms, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

18 citing papers in PubMed, 35 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

9 authors at 3 institutions in 1 country.

Yunting ZhouDepartment of Pediatrics, The Second Affiliated Hospital of Shantou University Medical College, Shantou 515041, China.
Qi HuDepartment of Pediatrics, The Second Affiliated Hospital of Shantou University Medical College, Shantou 515041, China.
Fuyi ChenDepartment of Pediatrics, The Second Affiliated Hospital of Shantou University Medical College, Shantou 515041, China.
Juan ZhangDepartment of Pediatrics, The Second Affiliated Hospital of Shantou University Medical College, Shantou 515041, China.
Jincheng GuoDepartment of Molecular Pathology, Shantou University Medical College, Shantou 515041, China.
Hongwu WangDepartment of Pediatrics, The Second Affiliated Hospital of Shantou University Medical College, Shantou 515041, China.
Jiang GuDepartment of Molecular Pathology, Shantou University Medical College, Shantou 515041, China.
Lian MaDepartment of Pediatrics, The Women and Children's Hospital of Shenzhen University, Shenzhen 518122, China.
Guyu HoDepartment of Pediatrics, The Second Affiliated Hospital of Shantou University Medical College, Shantou 515041, China guyuh@yahoo.com.
Shantou University · CNSecond Affiliated Hospital of Shantou University Medical College · CNShenzhen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human umbilical cord matrix-derived stem cells (uMSCs), owing to their cellular and procurement advantages compared with mesenchymal stem cells derived from other tissue sources, are in clinical trials to treat type 1 (T1D) and type 2 diabetes (T2D). However, the therapeutic basis remains to be fully understood. The immunomodulatory property of uMSCs could explain the use in treating T1D; however, the mere immune modulation might not be sufficient to support the use in T2D. We thus tested whether uMSCs could exert direct trophic effects on β-cells. Infusion of uMSCs into chemically induced diabetic rats prevented hyperglycemic progression with a parallel preservation of islet size and cellularity, demonstrating the protective effect of uMSCs on β-cells. Mechanistic analyses revealed that uMSCs engrafted long-term in the injured pancreas and the engraftment markedly activated the pancreatic PI3K pathway and its downstream anti-apoptotic machinery. The pro-survival pathway activation was associated with the expression and secretion of β-cell growth factors by uMSCs, among which insulin-like growth factor 1 (IGF1) was highly abundant. To establish the causal relationship between the uMSC-secreted factors and β-cell survival, isolated rat islets were co-cultured with uMSCs in the transwell system. Co-culturing improved the islet viability and insulin secretion. Furthermore, reduction of uMSC-secreted IGF1 via siRNA knockdown diminished the protective effects on islets in the co-culture. Thus, our data support a model whereby uMSCs exert trophic effects on islets by secreting β-cell growth factors such as IGF1. The study reveals a novel therapeutic role of uMSCs and suggests that multiple mechanisms are employed by uMSCs to treat diabetes.

Indexed as

Stem Cell TransplantationAnimalsCell SurvivalCoculture TechniquesDiabetes Mellitus, ExperimentalDisease ProgressionExtracellular MatrixGene Expression RegulationHumansHyperglycemiaInsulin-Like Growth Factor IInsulin-Secreting CellsPhosphatidylinositol 3-KinasesRats, Sprague-DawleyStem CellsStreptozocinInsulin-Like Growth Factor IPhosphatidylinositol 3-KinasesStreptozocinDiabetesGrowth factorsIGF1Stem cellsβ-cells

Identifiers

PMID26398949
PMCPMC4728317
OpenAlexW2341492543

What Socratic 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 Socratic graph.