Evidence map›Paper›PMID 23170111›Full record

ArticleExperimental and therapeutic medicine2012

Propranolol treatment of infantile hemangioma endothelial cells: A molecular analysis.

Jessica Stiles, Clarissa Amaya, Robert Pham, Rebecca K Rowntree, Mary Lacaze, Arlynn Mulne, Joyce Bischoff, Victor Kokta, Laura E Boucheron, Dianne C Mitchell and 1 more

Abstract read
In one paragraph

Article in Experimental and therapeutic medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

42 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Review
  5. Review
  6. Nanotechnology in Infantile Hemangioma Management.The journal of pediatric pharmacology and therapeutics : JPPT : the official journal of PPAG · 2025
    Article
  7. Review
  8. Article
  9. Article
  10. Infantile hemangioma: the common and enigmatic vascular tumor.The Journal of clinical investigation · 2024
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Infantile hemangiomas βPediatric research · 2022
    Article
  16. Review
  17. Propranolol inhibits stemness of hemangioma through Jagged1.Annals of translational medicine · 2021
    Article
  18. Critical role of Aquaporin-1 and telocytes in infantile hemangioma response to propranolol beta blockade.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  19. Article
  20. Review
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

11 authors.

Jessica StilesDepartment of Biomedical Sciences, Paul L. Foster School of Medicine, Texas Tech University Health Sciences Center, El Paso, TX;
Clarissa Amaya
Robert Pham
Rebecca K Rowntree
Mary Lacaze
Arlynn Mulne
Joyce Bischoff
Victor Kokta
Laura E Boucheron
Dianne C Mitchell
Brad A Bryan

Funding

Pathogenic mechanisms of venous anomaliesP01AR048564 · NIAMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI OLSEN, BJORN REINO · 2003 to 2013
$13.4M
The Role of VEGF-stimulated Rhoa/ROCK2 Signaling in Blood Vessel FormationR15HL098931 · NHLBI · WORCESTER STATE COLLEGE · PI BRYAN, BRAD ALLEN · 2010 to 2010
$206k
NHLBI NIH HHS R15 HL098931NIAMS NIH HHS P01 AR048564
6 · The paper itself

Abstract

Infantile hemangiomas (IHs) are non-malignant, largely cutaneous vascular tumors affecting approximately 5-10% of children to varying degrees. During the first year of life, these tumors are strongly proliferative, reaching an average size ranging from 2 to 20 cm. These lesions subsequently stabilize, undergo a spontaneous slow involution and are fully regressed by 5 to 10 years of age. Systemic treatment of infants with the non-selective β-adrenergic receptor blocker, propranolol, has demonstrated remarkable efficacy in reducing the size and appearance of IHs. However, the mechanism by which this occurs is largely unknown. In this study, we sought to understand the molecular mechanisms underlying the effectiveness of β blocker treatment in IHs. Our data reveal that propranolol treatment of IH endothelial cells, as well as a panel of normal primary endothelial cells, blocks endothelial cell proliferation, migration, and formation of the actin cytoskeleton coincident with alterations in vascular endothelial growth factor receptor-2 (VEGFR-2), p38 and cofilin signaling. Moreover, propranolol induces major alterations in the protein levels of key cyclins and cyclin-dependent kinase inhibitors, and modulates global gene expression patterns with a particular affect on genes involved in lipid/sterol metabolism, cell cycle regulation, angiogenesis and ubiquitination. Interestingly, the effects of propranolol were endothelial cell-type independent, affecting the properties of IH endothelial cells at similar levels to that observed in neonatal dermal microvascular and coronary artery endothelial cells. This data suggests that while propranolol markedly inhibits hemangioma and normal endothelial cell function, its lack of endothelial cell specificity hints that the efficacy of this drug in the treatment of IHs may be more complex than simply blockage of endothelial function as previously believed.

Identifiers

PMID23170111
PMCPMC3501380

What OpenQuestion holds

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Registered trials

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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.