Evidence map›Paper›PMID 19196827›Full record

ArticleCardiovascular research2009

A novel CXCR4 antagonist derived from human SDF-1beta enhances angiogenesis in ischaemic mice.

Yi Tan, Yan Li, Jian Xiao, Hongwei Shao, Chuanlin Ding, Gavin E Arteel, Keith A Webster, Jun Yan, Hong Yu, Lu Cai and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Cardiovascular research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

23 citing papers in PubMed, 55 citations in OpenAlex.

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  17. CXC chemokine receptor-4 signaling limits hepatocyte proliferation after hepatic ischemia-reperfusion in mice.American journal of physiology. Gastrointestinal and liver physiology · 2015
    Article
  18. Cardiac regeneration and diabetes.Regenerative medicine research · 2014
    Review
  19. Article
  20. Article
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

11 authors at 3 institutions in 2 countries.

Yi TanChinese-American Research Institute for Diabetic Complications, Wenzhou Medical College, Chashan College Park, Wenzhou 325035, China.
Yan Li
Jian Xiao
Hongwei Shao
Chuanlin Ding
Gavin E Arteel
Keith A Webster
Jun Yan
Hong Yu
Lu Cai
Xiaokun Li
University of Louisville · USUniversity of Miami · USWenzhou Medical University · CN

Funding

Regulated Therapeutic Angiogenesis: for Ischemic DiseaseR01HL072924 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI WEBSTER, KEITH A · 2003 to 2014
$3.2M
Bioengineering of a Stent-Graft for Gene TherapyR21HL076356 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI YU, HONG · 2004 to 2005
$417k
NHLBI NIH HHS HL 072924NHLBI NIH HHS HL 076356
6 · The paper itself

Abstract

aimsThe effects on angiogenesis of a novel CXC chemokine receptor 4 (CXCR4) antagonist, SDF-1betaP2G, derived from human stromal cell-derived factor-1beta (SDF-1beta), were examined in a model of hind limb ischaemia in mice. METHODS AND

resultsThe antagonistic activities of SDF-1betaP2G against CXCR4 were evaluated in vitro and in vivo and compared with phosphate-buffered saline and AMD3100 (a small bicyclam antagonist of SDF-1). Angiogenesis, muscle regeneration and the expression of pro-angiogenic factors were evaluated in ischaemic gastrocnemius muscles. Distant toxic effects of SDF-1betaP2G were evaluated by inflammatory and apoptotic markers. SDF-1betaP2G induced CXCR4 internalization and competitively inhibited the chemotaxis of SDF-1beta but did not mediate migration, calcium influx, or the phosphorylation of Akt and extracellular signal-regulated kinase in cultured T-lymphoblastic leukaemia cells or H9C2 cells. SDF-1betaP2G enhanced blood flow, angiogenesis, and muscle regeneration in ischaemic hind limbs, and the enhancement was significantly better than that of AMD3100. Markers of angiogenesis and progenitor cell migration, including phosphorylated Akt, vascular endothelial growth factor (VEGF), SDF-1 and CXCR4, were up-regulated by SDF-1betaP2G and co-localized with CD31-positive cells. Neutralization of VEGF with its specific antibody abolished SDF-1betaP2G-induced blood reperfusion and angiogenesis. No apparent inflammatory and apoptotic effects were found in heart, liver, kidneys, and testes after SDF-1betaP2G administration.

conclusionOur findings indicate that the novel CXCR4 antagonist, SDF-1betaP2G, can efficiently enhance ischaemic angiogenesis, blood flow restoration, and muscle regeneration without apparent adverse effects, most likely through a VEGF-dependent pathway.

Indexed as

Amino Acid SubstitutionAnimalsApoptosisCell Line, TumorChemokine CXCL12Escherichia coliHindlimbHumansInflammationIschemiaMaleMiceMuscle, SkeletalNeovascularization, PhysiologicRatsReceptors, CXCR4Chemokine CXCL12CXCL12 protein, humanReceptors, CXCR4Recombinant Proteins

Identifiers

PMID19196827
PMCPMC2682612
OpenAlexW2085368741

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.