Evidence map›Paper›PMID 22993248›Full record

ArticleJournal of the Royal Society, Interface2013

Regulation of endothelial MAPK/ERK signalling and capillary morphogenesis by low-amplitude electric field.

Abdul Q Sheikh, Toloo Taghian, Bryan Hemingway, Hongkwan Cho, Andrei B Kogan, Daria A Narmoneva

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the Royal Society, Interface, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

29 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
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  6. Article
  7. The bioelectrical properties of bone tissue.Animal models and experimental medicine · 2023
    Review
  8. Article
  9. Article
  10. Review
  11. Electroactive Biomaterials for Facilitating Bone Defect Repair under Pathological Conditions.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Review
  12. Review
  13. Extremely low frequency electromagnetic stimulation reduces ischemic stroke volume by improving cerebral collateral blood flow.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022
    Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Bioelectrical understanding and engineering of cell biology.Journal of the Royal Society, Interface · 2020
    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

6 authors at 1 institution in 1 country.

Abdul Q SheikhBiomedical Engineering, SEEBME, University of Cincinnati, 2901 Woodside Drive, Cincinnati, OH 45221-0012, USA.
Toloo Taghian
Bryan Hemingway
Hongkwan Cho
Andrei B Kogan
Daria A Narmoneva
University of Cincinnati · US

Funding

Angiogenic Peptide Scaffolds to Enhance Diabetic Wound HealingR21DK078814 · NIDDK · UNIVERSITY OF CINCINNATI · PI NARMONEVA, DARIA A. · 2008 to 2009
$460k
NIDDK NIH HHS 1R21DK078814-01A1NIDDK NIH HHS R21 DK078814
6 · The paper itself

Abstract

Low-amplitude electric field (EF) is an important component of wound-healing response and can promote vascular tissue repair; however, the mechanisms of action on endothelium remain unclear. We hypothesized that physiological amplitude EF regulates angiogenic response of microvascular endothelial cells via activation of the mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway. A custom set-up allowed non-thermal application of EF of high (7.5 GHz) and low (60 Hz) frequency. Cell responses following up to 24 h of EF exposure, including proliferation and apoptosis, capillary morphogenesis, vascular endothelial growth factor (VEGF) expression and MAPK pathways activation were quantified. A db/db mouse model of diabetic wound healing was used for in vivo validation. High-frequency EF enhanced capillary morphogenesis, VEGF release, MEK-cRaf complex formation, MEK and ERK phosphorylation, whereas no MAPK/JNK and MAPK/p38 pathways activation was observed. The endothelial response to EF did not require VEGF binding to VEGFR2 receptor. EF-induced MEK phosphorylation was reversed in the presence of MEK and Ca(2+) inhibitors, reduced by endothelial nitric oxide synthase inhibition, and did not depend on PI3K pathway activation. The results provide evidence for a novel intracellular mechanism for EF regulation of endothelial angiogenic response via frequency-sensitive MAPK/ERK pathway activation, with important implications for EF-based therapies for vascular tissue regeneration.

Indexed as

Electromagnetic FieldsMAP Kinase Signaling SystemMorphogenesisNeovascularization, PhysiologicAnimalsApoptosisCalciumCapillariesCell ProliferationCells, CulturedExtracellular Signal-Regulated MAP KinasesGene Expression RegulationMAP Kinase Kinase 4MicePhosphatidylinositol 3-KinasesPhosphorylationCalciumExtracellular Signal-Regulated MAP KinasesMAP Kinase Kinase 4Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-rafVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouse

Identifiers

PMID22993248
PMCPMC3565781
OpenAlexW2098749268

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.