Evidence map›Paper›PMID 29884909›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2019

ZBTB46 is a shear-sensitive transcription factor inhibiting endothelial cell proliferation via gene expression regulation of cell cycle proteins.

Yu Wang, He-Ying Sun, Sandeep Kumar, Maria Del Mar Puerta, Hanjoong Jo, Amir Rezvan

Open access · bronzeAbstract read
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 16% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Yu WangDepartment of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta, GA, USA.
He-Ying SunDepartment of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta, GA, USA.
Sandeep KumarDepartment of Medicine, Division of Cardiology, Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University School of Medicine, Atlanta, GA, USA.
Maria Del Mar PuertaDepartment of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta, GA, USA.
Hanjoong JoDepartment of Medicine, Division of Cardiology, Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University School of Medicine, Atlanta, GA, USA.ORCID http://orcid.org/0000-0003-1833-372X
Amir RezvanDepartment of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta, GA, USA. amir.rezvan@emory.edu.ORCID http://orcid.org/0000-0003-1229-5910
Emory University · USGeorgia Institute of Technology · US

Funding

T cell triggering events and hypertensionP01HL095070 · NHLBI · EMORY UNIVERSITY · PI GRIENDLING, KATHY K · 2009 to 2019
$20.5M
Role of flow-sensitive KLK10 in endothelial dysfunction and atherosclerosisR01HL139757 · NHLBI · EMORY UNIVERSITY · PI JO, HANJOONG · 2018 to 2021
$1.6M
The Role of zbtb46 in Endothelial Cell ActivationK08HL124292 · NHLBI · EMORY UNIVERSITY · PI REZVAN, AMIR · 2015 to 2019
$770k
NHLBI NIH HHS K08 HL124292NHLBI NIH HHS P01 HL095070NHLBI NIH HHS R01 HL139757
6 · The paper itself

Abstract

ZBTB46 is a transcription factor identified in classical dendritic cells and keeps dendritic cells in a quiescent state. Chromatin immunoprecipitation sequencing in dendritic cells has identified over 1300 potential gene targets of ZBTB46, affecting many processes including cell cycle. Endothelial cells (ECs) also express ZBTB46 and are mostly in a quiescent non-proliferative state. While EC proliferation is a critical process in development, dysregulation of EC proliferation as seen in areas of disturbed flow play an important role in many disease processes such as atherosclerosis, pulmonary hypertension, transplant vasculopathy, neointimal hyperplasia, and in-stent restenosis. We studied the role of ZBTB46 in ECs, hypothesizing that it inhibits EC proliferation. Using a model of disturbed flow in mice, we found that ZBTB46 is expressed in murine arterial ECs in vivo, and is downregulated by disturbed flow. In vitro results using HAECs showed that cell confluence and laminar shear stress, both known physiological conditions promoting EC quiescence, led to upregulation of ZBTB46 expression. Adenoviral-mediated overexpression of ZBTB46 in vitro caused reduced EC proliferation, and increased number of cells in the G

Indexed as

AnimalsApoptosisCell Cycle ProteinsCell NucleusCell ProliferationCells, CulturedCellular SenescenceDown-RegulationEndothelial CellsGene Expression RegulationHumansMaleMiceMice, Inbred C57BLNeovascularization, PhysiologicRetinoblastoma ProteinCell Cycle ProteinsRetinoblastoma ProteinRNA, MessengerRNA, Small InterferingTranscription FactorsZbtb46 protein, humanZbtb46 protein, mouse

Identifiers

PMID29884909
PMCPMC6286701
OpenAlexW2807057131

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.