Evidence map›Paper›PMID 28209985›Full record

ArticleExperimental & molecular medicine2017

Ig-like domain 6 of VCAM-1 is a potential therapeutic target in TNFα-induced angiogenesis.

Taek-Keun Kim, Chang Sik Park, Hee-Jun Na, Kangseung Lee, Aerin Yoon, Junho Chung, Sukmook Lee

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2017. 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
4.3field-weighted citation impact, top 6% 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, 43 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Experimental and therapeutic medicine · 2022
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. 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

7 authors at 2 institutions in 1 country.

Taek-Keun KimLaboratory of Molecular Cancer Therapeutics, Research Center, Scripps Korea Antibody Institute, Chuncheon, Republic of Korea.
Chang Sik ParkLaboratory of Molecular Cancer Therapeutics, Research Center, Scripps Korea Antibody Institute, Chuncheon, Republic of Korea.
Hee-Jun NaLaboratory of Molecular Cancer Therapeutics, Research Center, Scripps Korea Antibody Institute, Chuncheon, Republic of Korea.
Kangseung LeeLaboratory of Molecular Cancer Therapeutics, Research Center, Scripps Korea Antibody Institute, Chuncheon, Republic of Korea.
Aerin YoonDepartment of Biochemistry and Molecular Biology, College of Medicine, Seoul National University, Seoul, Republic of Korea.
Junho ChungDepartment of Biochemistry and Molecular Biology, College of Medicine, Seoul National University, Seoul, Republic of Korea.
Sukmook LeeLaboratory of Molecular Cancer Therapeutics, Research Center, Scripps Korea Antibody Institute, Chuncheon, Republic of Korea.
Scripps Korea Antibody Institute · KRSeoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor necrosis factor alpha (TNFα)-induced angiogenesis plays important roles in the progression of various diseases, including cancer, wet age-related macular degeneration, and rheumatoid arthritis. However, the relevance and role of vascular cell adhesion molecule-1 (VCAM-1) in angiogenesis have not yet been clearly elucidated. In this study, VCAM-1 knockdown shows VCAM-1 involvement in TNFα-induced angiogenesis. Through competitive blocking experiments with VCAM-1 Ig-like domain 6 (VCAM-1-D6) protein, we identified VCAM-1-D6 as a key domain regulating TNFα-induced vascular tube formation. We demonstrated that a monoclonal antibody specific to VCAM-1-D6 suppressed TNFα-induced endothelial cell migration and tube formation and TNFα-induced vessel sprouting in rat aortas. We also found that the antibody insignificantly affected endothelial cell viability, morphology and activation. Finally, the antibody specifically blocked VCAM-1-mediated cell-cell contacts by directly inhibiting VCAM-1-D6-mediated interaction between VCAM-1 molecules. These findings suggest that VCAM-1-D6 may be a potential novel therapeutic target in TNFα-induced angiogenesis and that antibody-based modulation of VCAM-1-D6 may be an effective strategy to suppress TNFα-induced angiogenesis.

Indexed as

Neovascularization, PhysiologicAnimalsAntibodies, MonoclonalCell MovementEndothelial CellsHEK293 CellsHumansHuman Umbilical Vein Endothelial CellsImmunoglobulin DomainsMaleRats, Sprague-DawleyTumor Necrosis Factor-alphaVascular Cell Adhesion Molecule-1Antibodies, MonoclonalTumor Necrosis Factor-alphaVascular Cell Adhesion Molecule-1

Identifiers

PMID28209985
PMCPMC5336558
OpenAlexW2587913523

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.