Evidence map›Paper›PMID 27669993›Full record

ArticleScientific reports2016

Flow-induced HDAC1 phosphorylation and nuclear export in angiogenic sprouting.

Despina Bazou, Mei Rosa Ng, Jonathan W Song, Shan Min Chin, Nir Maimon, Lance L Munn

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

26 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
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  7. Mechanical regulation of the early stages of angiogenesis.Journal of the Royal Society, Interface · 2022
    Review
  8. Article
  9. Article
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  11. Article
  12. Article
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  15. Article
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  17. High salt intake induces collecting duct HDAC1-dependent NO signaling.American journal of physiology. Renal physiology · 2021
    Article
  18. Cancers · 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

6 authors at 3 institutions in 1 country.

Despina BazouEdwin L. Steele Laboratories, Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, 100 Blossom Street, Boston, Massachusetts 02114, USA.
Mei Rosa NgEdwin L. Steele Laboratories, Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, 100 Blossom Street, Boston, Massachusetts 02114, USA.
Jonathan W SongDepartment of Mechanical and Aerospace Engineering, Ohio State University, E406 201 W. 19th Avenue, Columbus, OH 43210, USA.
Shan Min ChinEdwin L. Steele Laboratories, Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, 100 Blossom Street, Boston, Massachusetts 02114, USA.
Nir MaimonEdwin L. Steele Laboratories, Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, 100 Blossom Street, Boston, Massachusetts 02114, USA.
Lance L MunnEdwin L. Steele Laboratories, Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, 100 Blossom Street, Boston, Massachusetts 02114, USA.
Massachusetts General Hospital · USHarvard University · USThe Ohio State University · US

Funding

Targeting glycocalyx-mediated mechanisms of tumor metastasisR01CA204949 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI MUNN, LANCE L., TARBELL, JOHN M · 2017 to 2021
$2.3M
Encouraging anastomosis of engrafted vascular networksR01HL106584 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI MUNN, LANCE L. · 2012 to 2015
$1.3M
NCI NIH HHS R01 CA204949NHLBI NIH HHS R01 HL106584
6 · The paper itself

Abstract

Angiogenesis requires the coordinated growth and migration of endothelial cells (ECs), with each EC residing in the vessel wall integrating local signals to determine whether to remain quiescent or undergo morphogenesis. These signals include vascular endothelial growth factor (VEGF) and flow-induced mechanical stimuli such as interstitial flow, which are both elevated in the tumor microenvironment. However, it is not clear how VEGF signaling and mechanobiological activation due to interstitial flow cooperate during angiogenesis. Here, we show that endothelial morphogenesis is histone deacetylase-1- (HDAC1) dependent and that interstitial flow increases the phosphorylation of HDAC1, its activity, and its export from the nucleus. Furthermore, we show that HDAC1 inhibition decreases endothelial morphogenesis and matrix metalloproteinase-14 (MMP14) expression. Our results suggest that HDAC1 modulates angiogenesis in response to flow, providing a new target for modulating vascularization in the clinic.

Identifiers

PMID27669993
PMCPMC5037418
OpenAlexW2527591939

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.