Evidence map›Paper›PMID 28534977›Full record

ArticleInternational journal of molecular medicine2017

RUNX3 modulates hypoxia-induced endothelial-to-mesenchymal transition of human cardiac microvascular endothelial cells.

Yanhua Liu, Jin Zou, Bingong Li, Yuqin Wang, Delong Wang, Yanqin Hao, Xuan Ke, Xingxing Li

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.5field-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

25 citing papers in PubMed, 37 citations in OpenAlex.

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  9. Transcriptomic Context ofBiomedicines · 2023
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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

8 authors at 3 institutions in 1 country.

Yanhua LiuDepartment of Cardiology, The First Affiliated Hospital, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Jin ZouDepartment of Cardiology, The First Affiliated Hospital, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Bingong LiDepartment of Cardiology, The First Affiliated Hospital, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Yuqin WangDepartment of Cardiology, Loudi Central Hospital, Loudi, Hunan 417000, P.R. China.
Delong WangDepartment of Cardiology, Loudi Central Hospital, Loudi, Hunan 417000, P.R. China.
Yanqin HaoDepartment of Cardiology, The First Affiliated Hospital, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Xuan KeDepartment of Cardiology, The First Affiliated Hospital, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Xingxing LiDepartment of Cardiology, The First Affiliated Hospital, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
First Affiliated Hospital of Nanchang University · CNNanchang University · CNLoudi Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial-mesenchymal transition (EndMT) is an essential mechanism in the cardiovascular system, for both cardiovascular development and cardiovascular diseases (CVDs). Recent studies indicate that runt-related transcription factor 3 (RUNX3) contributes to EndMT and endothelial cell dysfunction. However, the underlying molecular mechanism remains unknown. The present study was designed to investigate the role of RUNX3 in EndMT and endothelial cell function, and to elucidate the underlying molecular mechanism. Human cardiac microvascular endothelial cells (HCMECs) were incubated in strictly controlled hypoxic conditions (1% O2). HCMECs were cultured under normoxic conditions (21% O2), and then moved to a strictly controlled hypoxic environment (1% O2). Under this hypoxic condition, the cells were transfected with the lentiviral vector containing RUNX3 or an empty lentiviral vector for 8 h. After the cells were cultured under hypoxic conditions for 4 days, CD31 and α-smooth muscle actin colocalization were assessed by immunofluorescence microscopy. Transwell migration and tube formation assays were used to examine the migration and angiogenesis ability. RT-qPCR and western blotting were used to determine the expression of molecules involved in EndMT. Hypoxia induced the transition of HCMECs to mesenchymal cells and markedly promoted tube formation and cell migration. Transforming growth factor-β (TGF-β) and Notch signaling were activated during the hypoxia-induced EndMT of HCMECs. RUNX3 knockdown attenuated EndMT of HCMECs, promoted angiogenic phenotype, and reduced endothelial cell migration. In conclusion, our results showed that RUNX3 knockdown attenuated hypoxia-induced EndMT and reversed endothelial cell functions. RUNX3 is a common downstream target of TGF-β and Notch signaling, and may be a novel therapeutic target for treating CVD mediated by EndMT.

Indexed as

Signal TransductionCell HypoxiaCore Binding Factor Alpha 3 SubunitCoronary VesselsEndothelial CellsHumansMicrovesselsReceptors, NotchTransforming Growth Factor betaCore Binding Factor Alpha 3 SubunitReceptors, NotchRunx3 protein, humanTransforming Growth Factor beta

Identifiers

PMID28534977
PMCPMC5466396
OpenAlexW2618908644

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.