Evidence map›Paper›PMID 32577545›Full record

ArticleHeliyon2020

Role of FOXM1 in vascular smooth muscle cell survival and neointima formation following vascular injury.

Sarah Franco, Amelia Stranz, Fiona Ljumani, Go Urabe, Mirnal Chaudhary, Danielle Stewart, Vijaya Satish Pilli, Matthew Kelly, Dai Yamanouchi, K Craig Kent and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Heliyon, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 43% 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

4 citing papers in PubMed, 7 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

11 authors at 1 institution in 1 country.

Sarah FrancoDepartment of Surgery, School of Medicine and Public Health, University of Wisconsin, Madison, WI 53705, USA.
Amelia StranzDepartment of Surgery, School of Medicine and Public Health, University of Wisconsin, Madison, WI 53705, USA.
Fiona LjumaniDepartment of Surgery, School of Medicine and Public Health, University of Wisconsin, Madison, WI 53705, USA.
Go UrabeDepartment of Surgery, School of Medicine and Public Health, University of Wisconsin, Madison, WI 53705, USA.
Mirnal ChaudharyDepartment of Surgery, School of Medicine and Public Health, University of Wisconsin, Madison, WI 53705, USA.
Danielle StewartDepartment of Surgery, School of Medicine and Public Health, University of Wisconsin, Madison, WI 53705, USA.
Vijaya Satish PilliDepartment of Surgery, School of Medicine and Public Health, University of Wisconsin, Madison, WI 53705, USA.
Matthew KellyDepartment of Surgery, School of Medicine and Public Health, University of Wisconsin, Madison, WI 53705, USA.
Dai YamanouchiDepartment of Surgery, School of Medicine and Public Health, University of Wisconsin, Madison, WI 53705, USA.
K Craig KentDepartment of Surgery, School of Medicine and Public Health, University of Wisconsin, Madison, WI 53705, USA.
Bo LiuDepartment of Surgery, School of Medicine and Public Health, University of Wisconsin, Madison, WI 53705, USA.
University of Wisconsin–Madison · US

Funding

Vascular Surgery Research Training ProgramT32HL110853 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI MATSUMURA, JON STEVEN · 2012 to 2021
$2.6M
Vascular smooth muscle cell apoptosis in intimal hyperplasiaR01HL122562 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI LIU, BO · 2015 to 2018
$1.6M
NHLBI NIH HHS R01 HL122562NHLBI NIH HHS T32 HL110853
6 · The paper itself

Abstract

backgroundAccelerated smooth muscle cell (SMC) proliferation is the primary cause of intimal hyperplasia (IH) following vascular interventions. Forkhead Box M1 (FOXM1) is considered a proliferation-associated transcription factor. However, the presence and role of FOXM1 in IH following vascular injury have not been determined.

objectiveWe examined the expression of FOXM1 in balloon-injured rat carotid arteries and investigated the effect of FOXM1 inhibition in SMCs and on the development of IH. METHODS AND

resultsFOXM1 was detected by immunofluorescent staining in balloon-injured rat carotid arteries where we observed an upregulation at day 7, 14, and 28 compared to uninjured controls. Immunofluorescence staining revealed FOXM1 coincided with proliferating cell nuclear antigen (PCNA). FOXM1 was also detectable in human carotid plaque samples. Western blot showed an upregulation of FOXM1 protein in serum-stimulated SMCs. Inhibition of FOXM1 using siRNA or chemical inhibition led to the induction of apoptosis as measured by flow cytometry and western blot for cleaved caspase 3. Perturbations in survival signaling were measured by western blot following FOXM1 inhibition, which showed a decrease in phosphorylated AKT and β-catenin. The chemical inhibitor thiostrepton was delivered by intraperitoneal injection in rats that underwent balloon injury and led to reduced intimal thickening compared to DMSO controls.

conclusionsFOXM1 is an important molecular mediator of IH that contributes to the proliferation and survival of SMCs following vascular injury.

Indexed as

ApoptosisBiological sciencesCell biologyFOXM1Intimal hyperplasiaMolecular biologyPathologyPathophysiologyProliferationSmooth muscle cell

Identifiers

PMID32577545
PMCPMC7303564
OpenAlexW3035810445

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.