Evidence map›Paper›PMID 21143386›Full record

ArticleJournal of cellular and molecular medicine2011

Defective CXCR4 expression in aged bone marrow cells impairs vascular regeneration.

Hongwei Shao, Qiyuan Xu, Qiuling Wu, Qi Ma, Luis Salgueiro, Jian'An Wang, Darwin Eton, Keith A Webster, Hong Yu

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular and molecular medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

26 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
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  3. Article
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  5. Review
  6. Role of Endothelial Progenitor Cells in Frailty.International journal of molecular sciences · 2023
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
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  15. Article
  16. Article
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  18. Vascular niche contribution to age-associated neural stem cell dysfunction.American journal of physiology. Heart and circulatory physiology · 2017
    Review
  19. Article
  20. Review
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

9 authors at 5 institutions in 2 countries.

Hongwei ShaoVascular Biology Institute, University of Miami, Miller School of Medicine, Miami, FL, USA.
Qiyuan Xu
Qiuling Wu
Qi Ma
Luis Salgueiro
Jian'An Wang
Darwin Eton
Keith A Webster
Hong Yu
University of Miami · USSecond Affiliated Hospital of Zhejiang University · CNMiami VA Healthcare System · USUnion Hospital · CNUniversity of Chicago · US

Funding

Regulated Therapeutic Angiogenesis: for Ischemic DiseaseR01HL072924 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI WEBSTER, KEITH A · 2003 to 2014
$3.2M
NHLBI NIH HHS R01 HL072924
6 · The paper itself

Abstract

The chemokine stromal cell-derived factor-1 (SDF-1) plays a critical role in mobilizing precursor cells in the bone marrow and is essential for efficient vascular regeneration and repair. We recently reported that calcium augments the expression of chemokine receptor CXCR4 and enhances the angiogenic potential of bone marrow derived cells (BMCs). Neovascularization is impaired by aging therefore we suggested that aging may cause defects of CXCR4 expression and cellular responses to calcium. Indeed we found that both the basal and calcium-induced surface expression of CXCR4 on BMCs was significantly reduced in 25-month-old mice compared with 2-month-old mice. Reduced Ca-induced CXCR4 expression in BMC from aged mice was associated with defective calcium influx. Diminished CXCR4 surface expression in BMC from aged mice correlated with diminished neovascularization in an ischemic hindlimb model with less accumulation of CD34(+) progenitor cells in the ischemic muscle with or without local overexpression of SDF-1. Intravenous injection of BMCs from old mice homed less efficiently to ischemic muscle and stimulated significantly less neovascularization compared with the BMCs from young mice. Transplantation of old BMCs into young mice did not reconstitute CXCR4 functions suggesting that the defects were not reversible by changing the environment. We conclude that defects of basal and calcium-regulated functions of the CXCR4/SDF-1 axis in BMCs contribute significantly to the age-related loss of vasculogenic responses.

Indexed as

RegenerationAnimalsBone Marrow CellsCalciumCellular SenescenceGene Expression RegulationHematopoietic Stem CellsHindlimbIschemiaMiceNeovascularization, PhysiologicReceptors, CXCR4Stem CellsVascular Endothelial Growth Factor ACalciumCXCR4 protein, humanReceptors, CXCR4Vascular Endothelial Growth Factor A

Identifiers

PMID21143386
PMCPMC3076550
OpenAlexW2077662795

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.