Evidence map›Paper›PMID 28266122›Full record

ArticleJournal of cellular and molecular medicine2017

Histone deacetylase inhibitors promote eNOS expression in vascular smooth muscle cells and suppress hypoxia-induced cell growth.

Xiaoling Tan, Lan Feng, Xiaoyong Huang, Yidong Yang, Chengzhong Yang, Yuqi Gao

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 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
0.9field-weighted citation impact, top 27% 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, 30 citations in OpenAlex.

  1. Article
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  5. Study of Transcriptomic Analysis of Yak (Animals : an open access journal from MDPI · 2023
    Article
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  7. Review
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  11. Article
  12. Review
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  14. Unconventional eNOS in pulmonary artery smooth muscles: why should it be there?Pflugers Archiv : European journal of physiology · 2019
    Article
  15. Article
  16. Review
  17. 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 2 institutions in 1 country.

Xiaoling TanDepartment of High Altitude Physiology & Biology, College of High Altitude Medicine, Third Military Medical University, Chongqing, China.
Lan FengDepartment of High Altitude Physiology & Biology, College of High Altitude Medicine, Third Military Medical University, Chongqing, China.
Xiaoyong HuangSouthwest Eye Hospital, Southwest Hospital, Third Military Medical University, Chongqing, China.
Yidong YangDepartment of Pathophysiology & High Altitude Pathology, College of High Altitude Medicine, Third Military Medical University, Chongqing, China.
Chengzhong YangDepartment of High Altitude Physiology & Biology, College of High Altitude Medicine, Third Military Medical University, Chongqing, China.
Yuqi GaoDepartment of Pathophysiology & High Altitude Pathology, College of High Altitude Medicine, Third Military Medical University, Chongqing, China.
Army Medical University · CNSouthwest Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxia stimulates excessive growth of vascular smooth muscle cells (VSMCs) contributing to vascular remodelling. Recent studies have shown that histone deacetylase inhibitors (HDIs) suppress VSMC proliferation and activate eNOS expression. However, the effects of HDI on hypoxia-induced VSMC growth and the role of activated eNOS in VSMCs are unclear. Using an EdU incorporation assay and flow cytometry analysis, we found that the HDIs, butyrate (Bur) and suberoylanilide hydroxamic acid (SAHA) significantly suppressed the proliferation of hypoxic VSMC lines and induced apoptosis. Remarkable induction of cleaved caspase 3, p21 expression and reduction of PCNA expression were also observed. Increased eNOS expression and enhanced NO secretion by hypoxic VSMC lines were detected using Bur or SAHA treatment. Knockdown of eNOS by siRNA transfection or exposure of hypoxic VSMCs to NO scavengers weakened the effects of Bur and SAHA on the growth of hypoxic VSMCs. In animal experiments, administration of Bur to Wistar rats exposed to hypobaric hypoxia for 28 days ameliorated the thickness and collagen deposition in pulmonary artery walls. Although the mean pulmonary arterial pressure (mPAP) was not obviously decreased with Bur in hypoxic rats, right ventricle hypertrophy index (RVHI) was decreased and the oxygen partial pressure of arterial blood was elevated. Furthermore, cell viability was decreased and eNOS and cleaved caspase 3 were induced in HDI-treated rat pulmonary arterial SMCs. These findings imply that HDIs prevent hypoxia-induced VSMC growth, in correlation with activated eNOS expression and activity in hypoxic VSMCs.

Indexed as

AnimalsApoptosisBenzoatesButyratesCell HypoxiaCell ProliferationHistone Deacetylase InhibitorsHydroxamic AcidsHypoxiaImidazolesMaleModels, BiologicalMuscle, Smooth, VascularMyocytes, Smooth MuscleNitric OxideNitric Oxide Synthase Type III1,3-dihydroxy-4,4,5,5-tetramethyl-2-(4-carboxyphenyl)tetrahydroimidazoleBenzoatesButyratesHistone Deacetylase InhibitorsHydroxamic AcidsImidazolesNitric OxideNitric Oxide Synthase Type IIIVorinostatendothelial nitric oxide synthasehistone deacetylase inhibitorhypoxiavascular remodellingvascular smooth muscle cell

Identifiers

PMID28266122
PMCPMC5571528
OpenAlexW2593609484

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.