Evidence map›Paper›PMID 29037123›Full record

ArticleAntioxidants & redox signaling2018

Ultrafine Particle Exposure Reveals the Importance of FOXO1/Notch Activation Complex for Vascular Regeneration.

Kyung In Baek, René R Sevag Packard, Jeffrey J Hsu, Arian Saffari, Zhao Ma, Anh Phuong Luu, Andrew Pietersen, Hilary Yen, Bin Ren, Yichen Ding and 3 more

Open access · greenAbstract read
In one paragraph

Article in Antioxidants & redox signaling, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

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  6. Ferroptosis: mechanisms and advances in ocular diseases.Molecular and cellular biochemistry · 2023
    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

13 authors at 3 institutions in 1 country.

Kyung In Baek1 Department of Bioengineering, University of California , Los Angeles, Los Angeles, California.
René R Sevag Packard2 Division of Cardiology, Department of Medicine, University of California , Los Angeles, Los Angeles, California.
Jeffrey J Hsu2 Division of Cardiology, Department of Medicine, University of California , Los Angeles, Los Angeles, California.
Arian Saffari3 Department of Civil and Environmental Engineering, University of Southern California , Los Angeles, California.
Zhao Ma1 Department of Bioengineering, University of California , Los Angeles, Los Angeles, California.
Anh Phuong Luu2 Division of Cardiology, Department of Medicine, University of California , Los Angeles, Los Angeles, California.
Andrew Pietersen1 Department of Bioengineering, University of California , Los Angeles, Los Angeles, California.
Hilary Yen1 Department of Bioengineering, University of California , Los Angeles, Los Angeles, California.
Bin Ren4 Division of Hematology and Oncology, Medical College of Wisconsin , Milwaukee, Wisconsin.
Yichen Ding2 Division of Cardiology, Department of Medicine, University of California , Los Angeles, Los Angeles, California.
Constantinos Sioutas3 Department of Civil and Environmental Engineering, University of Southern California , Los Angeles, California.
Rongsong Li2 Division of Cardiology, Department of Medicine, University of California , Los Angeles, Los Angeles, California.
Tzung K Hsiai1 Department of Bioengineering, University of California , Los Angeles, Los Angeles, California.
University of California, Los Angeles · USUniversity of Southern California · USMedical College of Wisconsin · US

Funding

CARDIOVASCULAR SCIENTIST TRAINING PROGRAMT32HL007895 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SHIVKUMAR, KALYANAM, WATSON, KAROL E · 1998 to 2023
$9.2M
Linking Spatial Variations Shear Stress-Oxidative StressR01HL083015 · NHLBI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI HSIAI, TZUNG K · 2006 to 2015
$3.9M
Shear Stress and Light-Sheets to Study Cardiac TrabeculationR01HL129727 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI HSIAI, TZUNG K, MARSDEN, ALISON L · 2015 to 2024
$3.5M
Electronica Impedance to Access Metabolically Active PlaqueR01HL118650 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI HSIAI, TZUNG K · 2014 to 2022
$3.3M
Micro-Sensors to Study Electrical and Mechanical Coupling of Injured MyocardiumR01HL111437 · NHLBI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI HSIAI, TZUNG K, XU, XIAOLEI · 2012 to 2020
$3.1M
NHLBI NIH HHS R01 HL083015NHLBI NIH HHS R01 HL111437NHLBI NIH HHS R01 HL118650NHLBI NIH HHS R01 HL129727NHLBI NIH HHS T32 HL007895
6 · The paper itself

Abstract

aimsRedox active ultrafine particles (UFP, d < 0.2 μm) promote vascular oxidative stress and atherosclerosis. Notch signaling is intimately involved in vascular homeostasis, in which forkhead box O1 (FOXO1) acts as a co-activator of the Notch activation complex. We elucidated the importance of FOXO1/Notch transcriptional activation complex to restore vascular regeneration after UFP exposure.

resultsIn a zebrafish model of tail injury and repair, transgenic Tg(fli1:GFP) embryos developed vascular regeneration at 3 days post amputation (dpa), whereas UFP exposure impaired regeneration (p < 0.05, n = 20 for control, n = 28 for UFP). UFP dose dependently reduced Notch reporter activity and Notch signaling-related genes (Dll4, JAG1, JAG2, Notch1b, Hey2, Hes1; p < 0.05, n = 3). In the transgenic Tg(tp1:GFP; flk1:mCherry) embryos, UFP attenuated endothelial Notch activity at the amputation site (p < 0.05 vs. wild type [WT], n = 20). A disintegrin and metalloproteinase domain-containing protein 10 (ADAM10) inhibitor or dominant negative (DN)-Notch1b messenger RNA (mRNA) disrupted the vascular network, whereas notch intracellular cytoplasmic domain (NICD) mRNA restored the vascular network (p < 0.05 vs. WT, n = 20). UFP reduced FOXO1 expression, but not Master-mind like 1 (MAML1) or NICD (p < 0.05, n = 3). Immunoprecipitation and immunofluorescence demonstrated that UFP attenuated FOXO1-mediated NICD pull-down and FOXO1/NICD co-localization, respectively (p < 0.05, n = 3). Although FOXO1 morpholino oligonucleotides (MOs) attenuated Notch activity, FOXO1 mRNA reversed UFP-mediated reduction in Notch activity to restore vascular regeneration and blood flow (p < 0.05 vs. WT, n = 5). Innovation and Conclusion: Our findings indicate the importance of the FOXO1/Notch activation complex to restore vascular regeneration after exposure to the redox active UFP. Antioxid. Redox Signal. 28, 1209-1223.

Indexed as

AnimalsCells, CulturedEndothelial CellsForkhead Box Protein O1Oxidation-ReductionParticulate MatterReceptors, NotchRegenerationRNA, MessengerZebrafishZebrafish ProteinsForkhead Box Protein O1foxo1a protein, zebrafishParticulate MatterReceptors, NotchRNA, MessengerZebrafish ProteinsFOXO1Notch signalingtail amputationUFPultrafine particlesvascular repair

Identifiers

PMID29037123
PMCPMC5912723
OpenAlexW2767072475

What OpenQuestion holds

Textmetadata
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.