Evidence map›Paper›PMID 32556532›Full record

ArticleActa diabetologica2020

Exendin-4 reverses high glucose-induced endothelial progenitor cell dysfunction via SDF-1β/CXCR7-AMPK/p38-MAPK/IL-6 axis.

Yong Yang, Yong Zhou, Yiyong Wang, Xianglong Wei, Lihao Wu, Tingzhong Wang, Aiqun Ma

Abstract read
PubMed Publisher
In one paragraph

Article in Acta diabetologica, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

17 citing papers in PubMed, 29 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

7 authors at 5 institutions in 2 countries.

Yong Yang *Department of Cardiovascular Internal Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, No. 277, West Yanta Road, Xi'an, Shaanxi, China.
Yong Zhou *Department of Oncology, The University of Hong Kong-Shenzhen Hospital, Shenzhen, Guangdong, China.
Yiyong WangDepartment of Cardiovascular Medicine, General Hospital of Ningxia Medical University, Yinchuan, Ningxia, China.
Xianglong WeiDepartment of Cardiovascular Internal Medicine, Shenzhen Hospital of Southern Medical University, Shenzhen, Guangdong, China.
Lihao WuDepartment of Cardiovascular Medicine, University of Chinese Academy of Science Shenzhen Hospital, Shenzhen, Guangdong, China.
Tingzhong WangDepartment of Cardiovascular Internal Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, No. 277, West Yanta Road, Xi'an, Shaanxi, China.
Aiqun MaDepartment of Cardiovascular Internal Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, No. 277, West Yanta Road, Xi'an, Shaanxi, China. maiqun_maaiqun@163.com.ORCID http://orcid.org/0000-0002-2527-8688
First Affiliated Hospital of Xi'an Jiaotong University · CNChinese University of Hong Kong, Shenzhen · CNNingxia Medical University · CNSouthern Medical University Shenzhen Hospital · CNUniversity of Hong Kong - Shenzhen Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimExendin-4, a glucagon-like peptide-1 (GLP-1) analog, has been used for treating diabetes mellitus (DM). However, its effects on improving the dysfunction of high glucose (HG)-induced endothelial progenitor cells (EPCs) remain unclear. The present study explored the effects of Exendin-4 on improving dysfunction of EPCs and the underlying mechanism.

methodsEPCs were isolated from SD rats and identified by flow cytometry. Next, the EPCs were treated by HG and high or low concentration of Exendin-4, and cell viability, migration and tube formation were, respectively, examined by performing MTT assay, wound-healing assay and tube formation assay. Interleukin-6 (IL-6) secretion was measured by enzyme-linked immunosorbent assay (ELISA). The protein expressions of relative stromal-derived growth factor-1β (SDF-1β), C-X-C chemokine receptor type 7 (CXCR7), AMP-activated protein kinase (AMPK), p38 and expressions of CXCR7 and IL-6 in EPCs were measured by Western blot. The cell behaviors of EPCs treated by HG and Exendin-4 with or without silencing of CXCR7 and IL-6 were detected.

resultsExendin-4 reversed the inhibitory effects of HG on viability, migration and tube formation of EPCs and on SDF-1β/CXCR7-AMPK pathway in EPCs in a dose-dependent manner. Moreover, Exendin-4 promoted the effects of HG on IL-6 level in EPCs through the promotion of p38-MAPK phosphorylation and reduction of cleaved caspase-3 protein expressions in EPCs. However, silencing of CXCR7 and IL-6 reversed the effects of Exendin-4 on cell behaviors, inactivated SDF-1β/CXCR7-AMPK pathway and increased cleaved caspase-3 expression in EPCs.

conclusionsExendin-4 could ameliorate HG-induced EPC dysfunction through regulating the production of IL-6 via SDF-1β/CXCR7-AMPK/p38-MAPK axis.

Indexed as

AMP-Activated Protein KinasesAnimalsCell SurvivalChemokine CXCL12Endothelial Progenitor CellsExenatideGlucoseHumansInterleukin-1betaInterleukin-6Malep38 Mitogen-Activated Protein KinasesPhosphorylationRatsRats, Sprague-DawleyReceptors, CXCRAckr3 protein, ratAMP-Activated Protein KinasesChemokine CXCL12ExenatideGlucoseInterleukin-1betaInterleukin-6p38 Mitogen-Activated Protein KinasesReceptors, CXCRDiabetes mellitusEndothelial progenitor cell dysfunctionExendin-4Interleukin-6SDF-1β/CXCR7–AMPK/p38-MAPK axis

Identifiers

PMID32556532
OpenAlexW3036356809

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.