Evidence map›Paper›PMID 23918400›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

TNFSF15 inhibits vasculogenesis by regulating relative levels of membrane-bound and soluble isoforms of VEGF receptor 1.

Jian-Wei Qi, Ting-Ting Qin, Li-Xia Xu, Kun Zhang, Gui-Li Yang, Jie Li, Huai-Yuan Xiao, Zhi-Song Zhang, Lu-Yuan Li

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. 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
3.4field-weighted citation impact, top 7% 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, 51 citations in OpenAlex.

  1. Article
  2. Article
  3. TNFSF15 facilitates the differentiation of CD11bCancer biology & medicine · 2023
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Vascular precursor cells in tissue injury repair.Translational research : the journal of laboratory and clinical medicine · 2017
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. TNFSF15 Inhibits Blood Retinal Barrier Breakdown Induced by Diabetes.International journal of molecular sciences · 2016
    Article
  17. Article
  18. Article
  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

9 authors at 2 institutions in 1 country.

Jian-Wei QiState Key Laboratory of Medicinal Chemical Biology and Nankai University College of Pharmacy, and Tianjin Key Laboratory of Molecular Drug Research, Tianjin 300071, China.
Ting-Ting Qin
Li-Xia Xu
Kun Zhang
Gui-Li Yang
Jie Li
Huai-Yuan Xiao
Zhi-Song Zhang
Lu-Yuan Li
State Key Laboratory of Medicinal Chemical BiologyNankai University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mouse bone marrow-derived Lin(-)-Sca-1(+) endothelial progenitor cell (EPC) has pluripotent abilities such as supporting neovascularization. Vascular endothelial growth factor (VEGF) receptor 1 (VEGFR1) (Flt1) recognizes various VEGF isoforms and is critically implicated in a wide range of physiological and pathological settings, including vasculogenesis. Mouse EPC expresses two isoforms of VEGFR1: mFlt1, which transmits ligand-induced signals; and sFlt1, which acts as a negative regulator by sequestering ligands of VEGF receptors. How the relative levels of mFlt1 and sFlt1 are regulated is not yet clear. We report here that tumor necrosis factor superfamily 15 (TNFSF15) (also known as VEGI or TL1A), an endothelial cell-secreted cytokine, simultaneously promotes mFlt1 degradation and up-regulates sFlt1 expression in EPC, giving rise to disruption of VEGF- or PlGF-induced activation of eNOS and MAPK p38 and effective inhibition of VEGF-driven, EPC-supported vasculogenesis in a murine Matrigel implant model. TNFSF15 treatment of EPC cultures facilitates Akt deactivation-dependent, ubiquitin-assisted degradation of mFlt1 and stimulates sFlt1 expression by activating the PKC, Src, and Erk1/2 signaling pathway. Additionally, TNFSF15 promotes alternative splicing of the Flt1 gene in favor of sFlt1 production by down-regulating nuclear protein Jumonji domain-containing protein 6 (Jmjd6), thus alleviating Jmjd6-inhibited sFlt1 expression. These findings indicate that TNFSF15 is a key component of a molecular mechanism that negatively modulates EPC-supported vasculogenesis through regulation of the relative levels of mFlt1 and sFlt1 in EPC.

Indexed as

ProteolysisAlternative SplicingAnalysis of VarianceAnimalsBlotting, WesternCollagenDrug CombinationsEndothelial CellsGene Expression RegulationLamininLigandsMiceMicroscopy, FluorescenceNeovascularization, PhysiologicProtein IsoformsProteoglycansCollagenDrug CombinationsLamininLigandsmatrigelProtein IsoformsProteoglycansTnfsf15 protein, mouseTumor Necrosis Factor Ligand Superfamily Member 15Vascular Endothelial Growth Factor Receptor-1angiogenesisprotein degradation

Identifiers

PMID23918400
PMCPMC3752234
OpenAlexW2137855372

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.