Evidence map›Paper›PMID 28811579›Full record

ArticleScientific reports2017

CXCL12 enhances angiogenesis through CXCR7 activation in human umbilical vein endothelial cells.

Min Zhang, Lisha Qiu, Yanyan Zhang, Dongsheng Xu, Jialin C Zheng, Li Jiang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
4.9field-weighted citation impact, top 3% 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

51 citing papers in PubMed, 104 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

6 authors at 4 institutions in 2 countries.

Min ZhangDivision of Cardiology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, 1111 Xianxia Road, Shanghai, 200336, P.R. China.
Lisha QiuCenter for Neuroimmunology and Regenerative Therapy, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 20072, P.R. China.
Yanyan ZhangCenter for Neuroimmunology and Regenerative Therapy, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 20072, P.R. China.
Dongsheng XuState Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan, 430072, P.R. China. dxu0927@sina.cn.
Jialin C ZhengCenter for Neuroimmunology and Regenerative Therapy, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 20072, P.R. China. jialinzheng@tongji.edu.cn.
Li JiangDivision of Cardiology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, 1111 Xianxia Road, Shanghai, 200336, P.R. China. jiangli@shtrhospital.com.
Tongji University · CNTongren Hospital · CNUniversity of Nebraska Medical Center · USWuhan University · CN

Funding

Nebraska Center for VirologyP30GM103509 · NIGMS · UNIVERSITY OF NEBRASKA LINCOLN · PI WOOD, CHARLES · 2012 to 2014
$3.3M
Glutaminase and its neurotoxic link to HANDR01NS097195 · NINDS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI GENDELMAN, HOWARD E · 2016 to 2020
$1.5M
Glutaminase and its neurotoxic link to HANDR56NS041858 · NINDS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI ZHENG, JIALIN CHARLES · 2015 to 2015
$376k
NIGMS NIH HHS P30 GM103509NINDS NIH HHS R01 NS097195NINDS NIH HHS R56 NS041858
6 · The paper itself

Abstract

Angiogenesis is the process by which new vessels form from existing vascular networks. Human umbilical vein endothelial cells (HUVECs) may contribute to the study of vascular repair and angiogenesis. The chemokine CXCL12 regulates multiple cell functions, including angiogenesis, mainly through its receptor CXCR4. In contrast to CXCL12/CXCR4, few studies have described roles for CXCR7 in vascular biology, and the downstream mechanism of CXCR7 in angiogenesis remains unclear. The results of the present study showed that CXCL12 dose-dependently enhanced angiogenesis in chorioallantoic membranes (CAMs) and HUVECs. The specific activation of CXCR7 with TC14012 (a CXCR7 agonist) resulted in the significant induction of tube formation in HUVECs and in vivo. Further evidence suggested that CXCL12 induced directional polarization and migration in the HUVECs, which is necessary for tube formation. Moreover, CXCR7 translocalization was observed during the polarization of HUVECs in stripe assays. Finally, treatment with TC14012 also significantly increased PI3K/Akt phosphorylation, and tube formation was blocked by treating HUVECs with an Akt inhibitor. Overall, this study indicated that CXCL12-stimulated CXCR7 acts as a functional receptor to activate Akt for angiogenesis in HUVECs and that CXCR7 may be a potential target molecule for endothelial regeneration and repair after vascular injury.

Indexed as

Neovascularization, PhysiologicAnimalsCells, CulturedChemokine CXCL12Chick EmbryoHumansHuman Umbilical Vein Endothelial CellsPhosphatidylinositol 3-KinasesProtein BindingProto-Oncogene Proteins c-aktReceptors, CXCRSignal TransductionACKR3 protein, humanChemokine CXCL12CXCL12 protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, CXCR

Identifiers

PMID28811579
PMCPMC5557870
OpenAlexW2743569227

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.