Evidence map›Paper›PMID 23414097›Full record

ArticleJournal of cellular and molecular medicine2013

Novel transcriptional regulation of VEGF in inflammatory processes.

Xiaoren Tang, Yu Yang, Huaiping Yuan, Jian You, Marina Burkatovskaya, Salomon Amar

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2013. 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
1.3field-weighted citation impact, top 20% 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, 33 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Low-intensity treadmill exercise promotes rat dorsal wound healing.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2016
    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

6 authors at 1 institution in 2 countries.

Xiaoren TangCenter for Anti-Inflammatory Therapeutics, Boston University Goldman School of Dental Medicine, Boston, MA 02118, USA.
Yu Yang
Huaiping Yuan
Jian You
Marina Burkatovskaya
Salomon Amar
Boston University · US

Funding

Role of LITAF in Inflammatory ProcessesR01DE014079 · NIDCR · NEW YORK MEDICAL COLLEGE · PI AMAR, SALOMON · 2002 to 2016
$5.4M
NIDCR NIH HHS R01 DE014079NIDCR NIH HHS R01 DE14079
6 · The paper itself

Abstract

Vascular endothelial growth factor (VEGF) is a critical angiogenic factor affecting endothelial cells, inflammatory cells and neuronal cells. In addition to its well-defined positive role in wound healing, pathological roles for VEGF have been described in cancer and inflammatory diseases (i.e. atherosclerosis, rheumatoid arthritis, inflammatory bowel disease and osteoarthritis). Recently, we showed that transcription factors LITAF and STAT6B affected the inflammatory response. This study builds upon our previous results in testing the role of mouse LITAF and STAT6B in the regulation of VEGF-mediated processes. Cells cotransfected with a series of VEGF promoter deletions along with truncated forms of mLITAF and/or mSTAT6B identified a DNA binding site (between -338 and -305 upstream of the transcription site) important in LITAF and/or STAT6B-mediated transcriptional regulation of VEGF. LITAF and STAT6B corresponding protein sites were identified. In addition, siRNA-mediated knockdown of mLITAF and/or mSTAT6B leads to significant reduction in VEGF mRNA levels and inhibits LPS-induced VEGF secretion in mouse RAW 264.7 cells. Furthermore, VEGF treatment of mouse macrophage or endothelial cells induces LITAF/STAT6B nuclear translocation and cell migration. To translate these observations in vivo, VEGF164-soaked matrigel were implanted in whole-body LITAF-deficient animals (TamLITAF(-/-) ), wild-type mice silenced for STAT6B, and in respective control animals. Vessel formation was found significantly reduced in TamLITAF(-/-) as well as in STAT6B-silenced wild-type animals compared with control animals. The present data demonstrate that VEGF regulation by LITAF and/or STAT6B is important in angiogenesis signalling pathways and may be a useful target in the treatment of VEGF diseases.

Indexed as

Cell MovementGene Expression RegulationNeovascularization, PathologicAnimalsApoptosisBlotting, WesternCell AdhesionCell ProliferationCollagenDNA-Binding ProteinsDrug CombinationsEndothelium, VascularEnzyme-Linked Immunosorbent AssayFlow CytometryImmunoprecipitationInflammationCollagenDNA-Binding ProteinsDrug CombinationsLamininLipopolysaccharidesLitaf protein, mousematrigelMitogen-Activated Protein Kinase 14Nuclear ProteinsProteoglycansRNA, MessengerRNA, Small InterferingStat6 protein, mouseSTAT6 Transcription FactorTranscription FactorsVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouse

Identifiers

PMID23414097
PMCPMC3612137
OpenAlexW2007105251

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.