Evidence map›Paper›PMID 25889019›Full record

ArticleStem cell research & therapy2015

CCR5 facilitates endothelial progenitor cell recruitment and promotes the stabilization of atherosclerotic plaques in ApoE-/- mice.

Zhongwen Zhang, Jianjun Dong, Corrinne G Lobe, Peiyun Gong, Ju Liu, Lin Liao

Open access · goldAbstract read
In one paragraph

Article in Stem cell research & therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 2 pooled it
1.5field-weighted citation impact, top 18% 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

24 citing papers in PubMed, 2 syntheses or guidelines pooled it, 40 citations in OpenAlex.

  1. Pooled it
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  10. Exosome-Based Treatment for Atherosclerosis.International journal of molecular sciences · 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

6 authors at 3 institutions in 1 country.

Zhongwen ZhangDepartment of Medicine, Shandong Provincial Qianfoshan Hospital, Shandong University, 16766 Jingshi Road, Jinan, Shandong, 250014, China. zhangzhongwen521@126.com.
Jianjun DongDepartment of Medicine, Qilu Hospital of Shandong University, Wenhua Road, Jinan, 250012, China. dongjianjun@medmail.com.cn.
Corrinne G LobeMiami Mice Research Corp., 101 College Street, Toronto, Ontario, M5G 1 L7, Canada. corrinnelobe@gmail.com.
Peiyun GongDepartment of Medicine, Qilu Hospital of Shandong University, Wenhua Road, Jinan, 250012, China. gongpeiyunshanda@163.com.
Ju LiuMedical Research Center, Shandong Provincial Qianfoshan Hospital, Shandong University, 16766 Jingshi Road, Jinan, Shandong, 250014, China. ju.liu@sdu.edu.cn.
Lin LiaoDepartment of Medicine, Shandong Provincial Qianfoshan Hospital, Shandong University, 16766 Jingshi Road, Jinan, Shandong, 250014, China. liaolin@medmail.com.cn.
Qilu Hospital of Shandong University · CNShandong University · CNShandong Provincial QianFoShan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionUnstable atherosclerotic plaques are prone to rupture, which leads to atherothrombosis. Endothelial progenitor cells (EPCs) are bone marrow-derived precursor cells that may repair vascular injury in atherosclerosis. Chemokine (C-C motif) receptor 5 (CCR5) promotes mobilization of EPCs. In this study, we investigated the therapeutic potential of CCR5-overexpressing EPCs on plaque stabilization in an apolipoprotein E (ApoE)-/- mouse model.

methodsThe expression of CCR5 and its cognate ligand chemokine (C-C motif) ligand 5 (CCL5) was examined in atherosclerotic aortas of humans and mice by immunohistochemistry. Splenectomized ApoE-/- C57BL/6 J mice fed a high-fat diet for 24 weeks were intravenously injected with EPCs transfected with CCR5 overexpression lentivirus. The recruitment of EPCs over the atherosclerotic plaques was evaluated by immunofluorescence. The content of lipid, smooth muscle cells, monocytes/macrophages, and endothelial cells in atherosclerotic plaques was assayed by specific immunostaining. The serum levels of atherosclerosis-related inflammatory factors in ApoE-/- mice were measured by mouse atherosclerosis antibody array I.

resultsCCR5 and CCL5 are highly expressed in atherosclerotic plaques in both humans and mice. The ApoE-/- mice with CCR5-overexpressing EPC treatment demonstrated a more stable plaque formation with enhanced recruitment of EPC, reduced lipid, and macrophage content in the atherosclerotic plaques. CCR5-overexpressing EPC treatment also increased the content of endothelial cells and nitric oxide production in the plaques. In addition, the serum levels of interleukin-3 (IL-3), IL-5, IL-6, IL-13, CD40, and tumor necrosis factor-alpha and the plaque contents of IL-6 and matrix metalloproteinase-9 were reduced in mice with CCR5-overexpressing EPC treatment.

conclusionsThese findings suggest that CCR5 is a novel therapeutic target in EPC treatment for stabilization of atherosclerotic plaques.

Indexed as

AnimalsAortaApolipoproteins EAtherosclerosisCD40 AntigensCell MovementCells, CulturedChemokine CCL5Disease Models, AnimalEndothelial Progenitor CellsHumansInterleukin-13Interleukin-3Interleukin-5Interleukin-6MaleApolipoproteins ECcl5 protein, mouseCCR5 protein, mouseCD40 AntigensChemokine CCL5Interleukin-13Interleukin-3Interleukin-5Interleukin-6Matrix Metalloproteinase 9Receptors, CCR5Tumor Necrosis Factor-alpha

Identifiers

PMID25889019
PMCPMC4404610
OpenAlexW2104139517

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.