Evidence map›Paper›PMID 28807051›Full record

ArticleStem cell research & therapy2017

Mesenchymal stromal cells ameliorate oxidative stress-induced islet endothelium apoptosis and functional impairment via Wnt4-β-catenin signaling.

Lingshu Wang, Li Qing, He Liu, Na Liu, Jingting Qiao, Chen Cui, Tianyi He, Ruxing Zhao, Fuqiang Liu, Fei Yan and 6 more

Open access · goldAbstract read
In one paragraph

Article in Stem cell research & therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 6% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

  1. Pooled it
  2. WNT4 reprograms dental pulp stem cells to resist PANoptosis and rebuild neurogenic potential for facial nerve injury repair.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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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

16 authors at 3 institutions in 2 countries.

Lingshu WangDepartment of Endocrinology, Institute of Endocrinology and Metabolism, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, China.ORCID 0000-0001-5263-3633
Li QingDepartment of Endocrinology, Institute of Endocrinology and Metabolism, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, China.
He LiuDepartment of Endocrinology, Institute of Endocrinology and Metabolism, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, China.
Na LiuCollege of Public Health, Shandong University, Jinan, Shandong, 250012, China.
Jingting QiaoDepartment of Endocrinology, Institute of Endocrinology and Metabolism, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, China.
Chen CuiDepartment of Endocrinology, Institute of Endocrinology and Metabolism, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, China.
Tianyi HeDepartment of Endocrinology, Institute of Endocrinology and Metabolism, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, China.
Ruxing ZhaoDepartment of Endocrinology, Institute of Endocrinology and Metabolism, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, China.
Fuqiang LiuDepartment of Endocrinology, Institute of Endocrinology and Metabolism, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, China.
Fei YanDepartment of Endocrinology, Institute of Endocrinology and Metabolism, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, China.
Chuan WangDepartment of Endocrinology, Institute of Endocrinology and Metabolism, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, China.
Kai LiangDepartment of Endocrinology, Institute of Endocrinology and Metabolism, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, China.
Xinghong GuoDepartment of Endocrinology, Institute of Endocrinology and Metabolism, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, China.
Ying H ShenDivision of Cardiothoracic Surgery, Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, TX, USA.
Xinguo HouDepartment of Endocrinology, Institute of Endocrinology and Metabolism, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, China. houxinguo@medmail.com.cn.
Li ChenDepartment of Endocrinology, Institute of Endocrinology and Metabolism, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, China. chenli3@medmail.com.cn.
Qilu Hospital of Shandong University · CNBaylor College of Medicine · USShandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIslet dysfunction and destruction are the common cause for both type 1 and type 2 diabetes mellitus (T2DM). The islets of Langerhans are highly vascularized miniorgans, and preserving the structural integrity and full function of the microvascular endothelium is vital for protecting the islets from the infiltration of immune cells and secondary inflammatory attack. Mesenchymal stromal cell (MSC)-based therapies have been proven to promote angiogenesis of the islets; however, the underlying mechanism for the protective role of MSCs in the islet endothelium is still vague.

methodsIn this study, we used MS-1, a murine islet microvascular endothelium cell line, and an MSC-MS1 transwell culturing system to investigate the protective mechanism of rat bone marrow-derived MSCs under oxidative stress in vitro. Cell apoptosis was detected by TUNEL staining, annexin V/PI flow cytometry analysis, and cleaved caspase 3 western blotting analysis. Endothelial cell activation was determined by expression of intercellular cell adhesion molecule (ICAM) and vascular cell adhesion molecule (VCAM), as well as eNOS phosphorylation/activation. The changes of VCAM-1, eNOS, and the β-catenin expression were also tested in the isolated islets of T2DM rats infused with MSCs.

resultsWe observed that treating MS-1 cells with H

conclusionsOur observations provide evidence that the orchestration of the MSC-secreted Wnts could promote the survival and improve the endothelial function of the injured islet endothelium via activating the β-catenin-dependent Wnt signaling in target endothelial cells. This finding might inspire further in-vivo studies.

Indexed as

ApoptosisOxidative StressSignal TransductionAnimalsbeta CateninCell LineCell NucleusCoculture TechniquesDiabetes Mellitus, Type 2Diet, High-FatEndothelium, VascularGene Knockdown TechniquesHydrogen PeroxideHyperglycemiaIslets of LangerhansMesenchymal Stem Cellsbeta CateninHydrogen PeroxideStreptozocinWnt4 ProteinWnt-5a ProteinIslet endotheliumMesenchymal stromal cellWnt

Identifiers

PMID28807051
PMCPMC5557510
OpenAlexW2747310946

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Registered trials

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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.