Evidence map›Paper›PMID 18408167›Full record

ArticleBlood2008

An essential role for SRC-activated STAT-3 in 14,15-EET-induced VEGF expression and angiogenesis.

Sergey Y Cheranov, Manjula Karpurapu, Dong Wang, Baolin Zhang, Richard C Venema, Gadiparthi N Rao

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed
5.9field-weighted citation impact, top 4% 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

93 citing papers in PubMed, 127 citations in OpenAlex.

  1. General View of Arachidonic Acid (AA) Metabolism.Reviews of physiology, biochemistry and pharmacology · 2027
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  3. Soluble Epoxide Hydrolase Inhibitors Improve Cornea Alkali Wound Healing.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Importance of STAT3 signaling in preeclampsia (Review).International journal of molecular medicine · 2025
    Review
  9. Article
  10. Review
  11. Secreted Phospholipases A2: Drivers of Inflammation and Cancer.International journal of molecular sciences · 2024
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

33 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 1 country.

Sergey Y CheranovDepartment of Physiology, University of Tennessee Health Science Center, Memphis 38163, USA.
Manjula Karpurapu
Dong Wang
Baolin Zhang
Richard C Venema
Gadiparthi N Rao
University of Tennessee Health Science Center · USAugusta University · US

Funding

Non-COX Arachidonic Acid Metabolites and AngiogenesisR01HL074860 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI RAO, GADIPARTHI N · 2004 to 2020
$5.9M
NHLBI NIH HHS HL074860NHLBI NIH HHS R01 HL074860
6 · The paper itself

Abstract

To understand the molecular mechanisms underlying 14,15-epoxyeicosatrienoic acid (14,15-EET)-induced angiogenesis, here we have studied the role of signal transducer and activator of transcription-3 (STAT-3). 14,15-EET stimulated the tyrosine phosphorylation of STAT-3 and its translocation from the cytoplasm to the nucleus in human dermal microvascular endothelial cells (HDMVECs). Adenovirus-mediated delivery of dominant negative STAT-3 substantially inhibited 14,15-EET-induced HDMVEC migration, and tube formation and Matrigel plug angiogenesis. 14,15-EET activated Src, as measured by its tyrosine phosphorylation and blockade of its activation by adenovirus-mediated expression of its dominant negative mutant, significantly attenuated 14,15-EET-induced STAT-3 phosphorylation in HDMVECs and the migration and tube formation of these cells and Matrigel plug angiogenesis. 14,15-EET induced the expression of vascular endothelial cell growth factor (VEGF) in a time- and Src-STAT-3-dependent manner in HDMVECs. Transfac analysis of VEGF promoter revealed the presence of STAT-binding elements and 14,15-EET induced STAT-3 binding to this promoter in vivo, and this interaction was inhibited by suppression of Src-STAT-3 signaling. Neutralizing anti-VEGF antibodies completely blocked 14,15-EET-induced HDMVEC migration and tube formation and Matrigel plug angiogenesis. These results reveal that Src-dependent STAT-3-mediated VEGF expression is a major mechanism of 14,15-EET-induced angiogenesis.

Indexed as

8,11,14-Eicosatrienoic AcidAortaCell MovementCells, CulturedCollagenDrug CombinationsEndothelial CellsGene ExpressionHumansLamininMyocytes, Smooth MuscleNeovascularization, PhysiologicPhosphorylationProteoglycansSignal Transductionsrc-Family Kinases14,15-epoxy-5,8,11-eicosatrienoic acid8,11,14-Eicosatrienoic AcidCollagenDrug CombinationsLamininmatrigelProteoglycanssrc-Family KinasesSTAT3 protein, humanSTAT3 Transcription FactorVascular Endothelial Growth Factor AVEGFA protein, human

Identifiers

PMID18408167
PMCPMC2424155
OpenAlexW2036931610

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.