Evidence map›Paper›PMID 34642827›Full record

ArticleJournal of molecular histology2021

SDF-1 secreted by mesenchymal stem cells promotes the migration of endothelial progenitor cells via CXCR4/PI3K/AKT pathway.

Xiaoyi Wang, Huijiao Jiang, Lijiao Guo, Sibo Wang, Wenzhe Cheng, Longfei Wan, Zhongzhou Zhang, Lihang Xing, Qing Zhou, Xiongfeng Yang and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular histology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Review
  3. Dynamic Fibrous Hydrogels for Stem Cell Homing and In Situ Bone Regeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Bioactive materials forBioactive materials · 2024
    Review
  11. Endothelial progenitor cells in pregnancy-related diseases.Clinical science (London, England : 1979) · 2023
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
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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

13 authors at 3 institutions in 1 country.

Xiaoyi Wang *Department of Pediatric Hematology and Oncology, The First Affiliated Hospital of Zhengzhou University, No. 1 Jianshe East Road, Zhengzhou, 450052, Henan, China.
Huijiao Jiang *Laboratory of Translational Medicine, Medical School of Shihezi University, No. 59 North 2 Road, Shihezi, 832002, Xinjiang, China.
Lijiao Guo *Laboratory of Translational Medicine, Medical School of Shihezi University, No. 59 North 2 Road, Shihezi, 832002, Xinjiang, China.
Sibo WangLaboratory of Translational Medicine, Medical School of Shihezi University, No. 59 North 2 Road, Shihezi, 832002, Xinjiang, China.
Wenzhe ChengLaboratory of Translational Medicine, Medical School of Shihezi University, No. 59 North 2 Road, Shihezi, 832002, Xinjiang, China.
Longfei WanLaboratory of Translational Medicine, Medical School of Shihezi University, No. 59 North 2 Road, Shihezi, 832002, Xinjiang, China.
Zhongzhou ZhangLaboratory of Translational Medicine, Medical School of Shihezi University, No. 59 North 2 Road, Shihezi, 832002, Xinjiang, China.
Lihang XingLaboratory of Translational Medicine, Medical School of Shihezi University, No. 59 North 2 Road, Shihezi, 832002, Xinjiang, China.
Qing ZhouLaboratory of Translational Medicine, Medical School of Shihezi University, No. 59 North 2 Road, Shihezi, 832002, Xinjiang, China.
Xiongfeng YangLaboratory of Translational Medicine, Medical School of Shihezi University, No. 59 North 2 Road, Shihezi, 832002, Xinjiang, China.
Huanhuan HanLaboratory of Translational Medicine, Medical School of Shihezi University, No. 59 North 2 Road, Shihezi, 832002, Xinjiang, China.
Xueling ChenDepartment of Immunology, Medical School of Shihezi University, No. 59 North 2 Road, Shihezi, 832002, Xinjiang, China. chenxueling@shzu.cn.
Xiangwei WuLaboratory of Translational Medicine, Medical School of Shihezi University, No. 59 North 2 Road, Shihezi, 832002, Xinjiang, China. wxwshz@126.com.
Shihezi University · CNFirst Affiliated Hospital of Shihezi University Medical College · CNFirst Affiliated Hospital of Zhengzhou University · CN

Funding

National Natural Science Foundation of China 81602810National Natural Science Foundation of China 81703174National Natural Science Foundation of China 81760371the Autonomous Region Graduate Student Scientific Research Innovation Project XJ2019G081the National Natural Science Foundation of China 81760570the Project of Young and Middle-aged Scientific and Technological Innovation Leaders in Bingtuan 2018CB017
6 · The paper itself

Abstract

Cell-based therapeutics bring great hope in areas of unmet medical needs. Mesenchymal stem cells (MSCs) have been suggested to facilitate neovascularization mainly by paracrine action. Endothelial progenitor cells (EPCs) can migrate to ischemic sites and participate in angiogenesis. The combination cell therapy that includes MSCs and EPCs has a favorable effect on ischemic limbs. However, the mechanism of combination cell therapy remains unclear. Herein, we investigate whether stromal cell-derived factor (SDF)-1 secreted by MSCs contributes to EPC migration to ischemic sites via CXCR4/Phosphoinositide 3-Kinases (PI3K)/protein kinase B (termed as AKT) signaling pathway. First, by a "dual-administration" approach, intramuscular MSC injections were supplemented with intravenous Qdot® 525 labeled-EPC injections in the mouse model of hind limb ischemia. Then, the mechanism of MSC effect on EPC migration was detected by the transwell system, tube-like structure formation assays, western blot assays in vitro. Results showed that the combination delivery of MSCs and EPCs enhanced the incorporation of EPCs into the vasculature and increased the capillary density in mouse ischemic hind limb. The numbers of CXCR4-positive EPCs increased after incubation with MSC-conditioned medium (CM). MSCs contributed to EPC migration and tube-like structure formation, both of which were suppressed by AMD3100 and wortmannin. Phospho-AKT induced by MSC-CM was attenuated when EPCs were pretreated with AMD3100 and wortmannin. In conclusion, we confirmed that MSCs contributes to EPC migration, which is mediated via CXCR4/PI3K/AKT signaling pathway.

Indexed as

Signal TransductionAnimalsCell CommunicationCell MovementCells, CulturedChemokine CXCL12Disease Models, AnimalEndothelial Progenitor CellsExtremitiesImmunophenotypingIschemiaMesenchymal Stem CellsMesenchymal Stem Cell TransplantationMiceNeovascularization, PhysiologicPhosphatidylinositol 3-KinasesChemokine CXCL12Cxcl12 protein, mousePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, CXCR4AKTCXCR4Endothelial progenitor cellsMesenchymal stem cellsMouse model of hind limb ischemiaStromal cell-derived factor-1

Identifiers

PMID34642827
OpenAlexW3136778596

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.