Evidence map›Paper›PMID 33770315›Full record

ArticleMolecular and cellular biochemistry2021

CXCL1 stimulates decidual angiogenesis via the VEGF-A pathway during the first trimester of pregnancy.

Chao Ma, Guangxing Liu, Wei Liu, Wei Xu, Hongtu Li, Shuhua Piao, Yang Sui, Wenhua Feng

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular and cellular biochemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.8field-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

22 citing papers in PubMed, 32 citations in OpenAlex.

  1. The Significance of CXCL1 in Cancer: An Overview of Molecular Mechanisms.International journal of molecular sciences · 2026
    Review
  2. Article
  3. Review
  4. Chemokines in Pregnancy.Biomolecules · 2025
    Review
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  7. Observational
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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

8 authors at 1 institution in 1 country.

Chao MaKey Laboratory of Reproductive Health and Medical Genetics, National Health and Family Planning Commission, Liaoning Province Research Institute of Family Planning, China Medical University, 10 PuHe Street, Huanggu District, Shenyang, 110031, China.ORCID http://orcid.org/0000-0003-4378-1380
Guangxing LiuKey Laboratory of Reproductive Health and Medical Genetics, National Health and Family Planning Commission, Liaoning Province Research Institute of Family Planning, China Medical University, 10 PuHe Street, Huanggu District, Shenyang, 110031, China.
Wei LiuKey Laboratory of Reproductive Health and Medical Genetics, National Health and Family Planning Commission, Liaoning Province Research Institute of Family Planning, China Medical University, 10 PuHe Street, Huanggu District, Shenyang, 110031, China.
Wei XuKey Laboratory of Reproductive Health and Medical Genetics, National Health and Family Planning Commission, Liaoning Province Research Institute of Family Planning, China Medical University, 10 PuHe Street, Huanggu District, Shenyang, 110031, China.
Hongtu LiKey Laboratory of Reproductive Health and Medical Genetics, National Health and Family Planning Commission, Liaoning Province Research Institute of Family Planning, China Medical University, 10 PuHe Street, Huanggu District, Shenyang, 110031, China.
Shuhua PiaoKey Laboratory of Reproductive Health and Medical Genetics, National Health and Family Planning Commission, Liaoning Province Research Institute of Family Planning, China Medical University, 10 PuHe Street, Huanggu District, Shenyang, 110031, China.
Yang SuiKey Laboratory of Reproductive Health and Medical Genetics, National Health and Family Planning Commission, Liaoning Province Research Institute of Family Planning, China Medical University, 10 PuHe Street, Huanggu District, Shenyang, 110031, China.
Wenhua FengKey Laboratory of Reproductive Health and Medical Genetics, National Health and Family Planning Commission, Liaoning Province Research Institute of Family Planning, China Medical University, 10 PuHe Street, Huanggu District, Shenyang, 110031, China. whfeng111@126.com.
National Health and Family Planning Commission · CN

Funding

Natural Science Foundation of Liaoning Province 2018225087Natural Science Foundation of Liaoning Province (CN) 2019-ZD-1093Shenyang Young and Middle-aged Science and Technology Innovation Talent Support Project RC180301
6 · The paper itself

Abstract

Angiogenesis is critical to establishing a successful pregnancy. The chemokine (C-X-C motif) ligand 1 (CXCL1) is a small cytokine belonging to the CXC chemokine family that is an important chemokine involved in the processes of angiogenesis and arteriogenesis; however, little is known about its role in decidual angiogenesis. Effects of CXCL1 on cell proliferation and migration (propidium iodide staining and wound healing assays) of HUVEC cells were determined. The angiogenesis roles of CXCL1 in HUVEC-HTR8/SVneo co-culture system were detected by the tube formation assay. Signal transduction pathways in HUVEC cells in response to CXCL1 were determined by in-cell western analyses. In vivo, mice were injected with (1) PBS (Group A) or (2) CXCL1-neutralizing antibody (Group B) or (3) CXCL1-neutralizing antibody plus recombinant VEGF-A protein (Group C) from E1 to E5 and sacrificed at E6.5 of pregnancy. The decidual angiogenesis in mice was examined by immunohistochemistry of cluster designation 34 (CD34), and the expression levels of vascular endothelial growth factor-A (VEGF-A) in the decidual cells and vascular endothelial growth factor receptor 2 (VEGFR2) in decidual vascular endothelial cells were also tested. Exogenous recombinant human CXCL1 supported endothelial cell proliferation and migration, and this effect was blocked by CXCL1-neutralizing antibody or CXCR2 inhibitor SB265610. The tube formation of HUVEC-HTR8/SVneo co-culture system was significantly stimulated by CXCL1, but this effect was markedly abrogated once they were pretreated with CXCL1-neutralizing antibody or CXCR2 inhibitor SB265610. In addition, the level of vascular endothelial growth factor A (VEGF-A) expression in HUVEC cells was increased by CXCL1, and this level was suppressed by CXCL1-neutralizing antibody or CXCR2 inhibitor SB265610. In vivo, compared with Group A (n = 3), decidual angiogenesis was significantly reduced in Group B by CD34 immunostaining. But compared with Group B, decidual angiogenesis was significantly increased in Group C. In addition, the expression of VEGF-A and VEGFR2 was significantly increased after neutralizing of CXCL1 in Group B. In conclusions, CXCL1 may play essential roles in decidual angiogenesis during the first trimester, and this function may be mediated in part via altering VEGF-A expression.

Indexed as

Neovascularization, PhysiologicAnimalsCell MovementCell ProliferationChemokine CXCL1DeciduaFemaleHumansHuman Umbilical Vein Endothelial CellsMicePregnancyPregnancy Trimester, FirstSignal TransductionTrophoblastsVascular Endothelial Growth Factor AChemokine CXCL1Cxcl1 protein, mouseVascular Endothelial Growth Factor AAngiogenesisChemokine (C-X-C motif) ligand 1Endothelial cellsPregnancyVEGF-A

Identifiers

PMID33770315
OpenAlexW3138747175

What OpenQuestion holds

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Registered trials

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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.