Evidence map›Paper›PMID 28127553›Full record

ArticleBioMed research international2017

Role of Phosphorylated HDAC4 in Stroke-Induced Angiogenesis.

Juan Liu, Xiang Zhou, Qing Li, Shu-Min Zhou, Bin Hu, Guo-Wen Hu, Xin Niu, Shang-Chun Guo, Yang Wang, Zhi-Feng Deng

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
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  14. miR-149-5p Inhibits Vascular Smooth Muscle Cells Proliferation, Invasion, and Migration by Targeting Histone Deacetylase 4 (HDAC4).Medical science monitor : international medical journal of experimental and clinical research · 2019
    Article
  15. Autophagy Induced by Oxygen-Glucose Deprivation Mediates the Injury to the Neurovascular Unit.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Article
  16. Review
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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

10 authors at 2 institutions in 1 country.

Juan LiuDepartment of Neurosurgery, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Xiang ZhouDepartment of Neurosurgery, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China; Graduate School of Nanchang University, Nanchang, China.
Qing LiInstitute of Microsurgery on Extremities, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Shu-Min ZhouInstitute of Microsurgery on Extremities, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Bin HuInstitute of Microsurgery on Extremities, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Guo-Wen HuDepartment of Neurosurgery, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China; Graduate School of Nanchang University, Nanchang, China.
Xin NiuInstitute of Microsurgery on Extremities, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Shang-Chun GuoInstitute of Microsurgery on Extremities, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Yang WangInstitute of Microsurgery on Extremities, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.ORCID 0000-0003-0738-9621
Zhi-Feng DengDepartment of Neurosurgery, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.ORCID 0000-0003-3529-0549
Shanghai Jiao Tong University · CNNanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acetylation or deacetylation of chromatin proteins and transcription factors is part of a complex signaling system that is involved in the control of neurological disorders. Recent studies have demonstrated that histone deacetylases (HDACs) exert protective effects in attenuating neuronal injury after ischemic insults. Class IIa HDAC4 is highly expressed in the brain, and neuronal activity depends on the nucleocytoplasmic shuttling of HDAC4. However, little is known about HDAC4 and its roles in ischemic stroke. In this study, we report that phosphorylation of HDAC4 was remarkably upregulated after stroke and blockade of HDAC4 phosphorylation with GÖ6976 repressed stroke-induced angiogenesis. Phosphorylation of HDAC4 was also increased in endothelial cells hypoxia model and suppression of HDAC4 phosphorylation inhibited the tube formation and migration of endothelial cells in vitro. Furthermore, in addition to the inhibition of angiogenesis, blockade of HDAC4 phosphorylation suppressed the expression of genes downstream of HIF-VEGF signaling in vitro and in vivo. These data indicate that phosphorylated HDAC4 may serve as an important regulator in stroke-induced angiogenesis. The protective mechanism of phosphorylated HDAC4 is associated with HIF-VEGF signaling, implicating a novel therapeutic target in stroke.

Indexed as

Neovascularization, PhysiologicAnimalsBrainCarbazolesCells, CulturedDisease Models, AnimalEndothelial CellsHistone Deacetylase InhibitorsHistone DeacetylasesHypoxia-Inducible Factor 1, alpha SubunitMalePhosphorylationRatsRats, Sprague-DawleySignal TransductionStrokeCarbazolesGo 6976HDAC4 protein, ratHif1a protein, ratHistone Deacetylase InhibitorsHistone DeacetylasesHypoxia-Inducible Factor 1, alpha SubunitVascular Endothelial Growth Factor Avascular endothelial growth factor A, rat

Identifiers

PMID28127553
PMCPMC5239970
OpenAlexW2561023603

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.