Evidence map›Paper›PMID 26250571›Full record

ArticleScientific reports2015

Effects of Exendin-4 on bone marrow mesenchymal stem cell proliferation, migration and apoptosis in vitro.

Hao Zhou, Dandan Li, Chen Shi, Ting Xin, Junjie Yang, Ying Zhou, Shunyin Hu, Feng Tian, Jing Wang, Yundai Chen

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
8.3field-weighted citation impact, top 2% 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

58 citing papers in PubMed, 113 citations in OpenAlex.

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  12. Stem cell homing in periodontal tissue regeneration.Frontiers in bioengineering and biotechnology · 2022
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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

10 authors at 3 institutions in 1 country.

Hao ZhouDepartment of Cardiology, Chinese PLA General Hospital, Beijing, China.
Dandan LiDepartment of Cardiology, Chinese PLA General Hospital, Beijing, China.
Chen ShiDepartment of Radiotherapy, Beijing Cancer Hospital, Beijing, China.
Ting XinDepartment of Cardiology, Tianjin First Central Hospital, Tianjin, China.
Junjie YangDepartment of Cardiology, Chinese PLA General Hospital, Beijing, China.
Ying ZhouDepartment of Cardiology, Chinese PLA General Hospital, Beijing, China.
Shunyin HuDepartment of Cardiology, Chinese PLA General Hospital, Beijing, China.
Feng TianDepartment of Cardiology, Chinese PLA General Hospital, Beijing, China.
Jing WangDepartment of Cardiology, Chinese PLA General Hospital, Beijing, China.
Yundai ChenDepartment of Cardiology, Chinese PLA General Hospital, Beijing, China.
Chinese PLA General Hospital · CNPeking University Cancer Hospital · CNTianjin Medical University · CN

Funding

Impact of Prenatal Alcohol Exposure on Receptor Targeting and FunctioningR03AA020101 · NIAAA · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI CALDWELL, KEVIN K. · 2010 to 2011
$148k
NIAAA NIH HHS R03 AA020101
6 · The paper itself

Abstract

Mesenchymal stem cells (MSC) are regarded as an attractive source of therapeutic stem cells for myocardial infarction. However, their limited self-renewal capacity, low migration capacity and poor viability after transplantation hamper the clinical use of MSC; thus, a strategy to enhance the biological functions of MSC is required. Exendin-4 (Ex-4), a glucagon-like peptide-1 receptor agonist, exerts cell-protective effects on many types of cells. However, little information is available regarding the influence of Ex-4 on MSC. In our study, MSC were isolated from bone marrow and cultured in vitro. After treatment with Ex-4, MSC displayed a higher proliferative capacity, increased C-X-C motif receptor 4 (CXCR4) expression and an enhanced migration response. Moreover, in H2O2-induced apoptosis, Ex-4 preserved mitochondrial function through scavenging ROS and balancing the expression of anti- and pro-apoptotic proteins, leading to the inhibition of the mitochondria-dependent cell death pathways and increased cell survival. Moreover, higher phospho-Akt (p-Akt) expression was observed after Ex-4 intervention. However, blockade of the PI3K/Akt pathway with inhibitors suppressed the above cytoprotective effects of Ex-4, suggesting that the PI3K/Akt pathway is partly responsible for Ex-4-mediated MSC growth, mobilization and survival. These findings provide an attractive method of maximizing the effectiveness of MSC-based therapies in clinical applications.

Indexed as

AnimalsApoptosisApoptosis Regulatory ProteinsBone Marrow CellsCell MovementCell ProliferationCell SurvivalExenatideHydrogen PeroxideMesenchymal Stem CellsMitochondriaPeptidesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRatsRats, Sprague-DawleyApoptosis Regulatory ProteinsCxcr4 protein, ratExenatideHydrogen PeroxidePeptidesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReactive Oxygen SpeciesReceptors, CXCR4Venoms

Identifiers

PMID26250571
PMCPMC4528192
OpenAlexW1809361764

What OpenQuestion 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 OpenQuestion graph.