Evidence map›Paper›PMID 38908672›Full record

ArticleEnvironmental pollution (Barking, Essex : 1987)2024

Diesel exhaust particle extract elicits an oxPAPC-like transcriptomic profile in macrophages across multiple mouse strains.

May Bhetraratana, Luz D Orozco, Brian J Bennett, Karla Luna, Xia Yang, Aldons J Lusis, Jesus A Araujo

Abstract read
In one paragraph

Article in Environmental pollution (Barking, Essex : 1987), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

7 authors.

May BhetraratanaDivision of Cardiology, Department of Medicine, David Geffen School of Medicine at UCLA, 10833 Le Conte Ave., Los Angeles, CA, 90095, USA.
Luz D OrozcoDepartment of Human Genetics, David Geffen School of Medicine at UCLA, 10833 Le Conte Ave., Los Angeles, CA, 90095, USA.
Brian J BennettDivision of Cardiology, Department of Medicine, David Geffen School of Medicine at UCLA, 10833 Le Conte Ave., Los Angeles, CA, 90095, USA.
Karla LunaDivision of Cardiology, Department of Medicine, David Geffen School of Medicine at UCLA, 10833 Le Conte Ave., Los Angeles, CA, 90095, USA; Department of Biology, College of Science and Math, California State University-Northridge, 18111 Nordhoff Street, Northridge, CA, 91330, USA.
Xia YangDepartment of Integrative Biology and Physiology, UCLA, 612 Charles E. Young Drive East, Los Angeles, CA, 90095, USA; Institute for Quantitative and Computational Biosciences, UCLA, 610 Charles E. Young Drive East, Los Angeles, CA, 90095, USA; Molecular Biology Institute, UCLA, 611 Charles E. Young Drive East, Los Angeles, CA, 90095, USA.
Aldons J LusisDivision of Cardiology, Department of Medicine, David Geffen School of Medicine at UCLA, 10833 Le Conte Ave., Los Angeles, CA, 90095, USA; Department of Human Genetics, David Geffen School of Medicine at UCLA, 10833 Le Conte Ave., Los Angeles, CA, 90095, USA; Molecular Biology Institute, UCLA, 611 Charles E. Young Drive East, Los Angeles, CA, 90095, USA.
Jesus A AraujoDivision of Cardiology, Department of Medicine, David Geffen School of Medicine at UCLA, 10833 Le Conte Ave., Los Angeles, CA, 90095, USA; Molecular Biology Institute, UCLA, 611 Charles E. Young Drive East, Los Angeles, CA, 90095, USA; Department of Environmental Health Sciences, Fielding School of Public Health, UCLA, 650 Charles E. Young Dr. South, Los Angeles, CA, 90095, USA. Electronic address: JAraujo@mednet.ucla.edu.

Funding

Training in Molecular ToxicologyT32ES015457 · NIEHS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ALLARD, PATRICK, HANKINSON, OLIVER NMN · 2008 to 2025
$4.0M
Dissecting the Role of Arachidonic Acid Metabolic Pathways Involved in Resolution Versus Progression of PM-Induced Cardiometabolic ToxicityR01ES033703 · NIEHS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Jesus Antonio Araujo · 2022 to 2026
$3.3M
Systems genetics approach to inflammatory mechanisms in atherosclerosisR01HL147883 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LUSIS, ALDONS JAKE · 2019 to 2022
$3.0M
Effects of particulate air pollution on HDL function and atherosclerosisR01ES016959 · NIEHS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ARAUJO, JESUS ANTONIO · 2009 to 2013
$2.4M
Role of Intestinal Microbiota in Dyslipidemia and Atherosclerosis Induced by Ambient Ultrafine ParticlesR01ES029395 · NIEHS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ARAUJO, JESUS ANTONIO, HSIAI, TZUNG K · 2018 to 2022
$2.2M
Interplay Between Macrophages, Lipid Oxidation and the Nrf2/HO-1 Axis in the Cardiometabolic Toxicity Induced by Ultrafine ParticlesR01ES032806 · NIEHS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ARAUJO, JESUS ANTONIO · 2021 to 2025
$2.0M
Effects of particulate air pollution on HDL function and athersclerosisR56ES016959 · NIEHS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ARAUJO, JESUS ANTONIO · 2014 to 2014
$154k
NHLBI NIH HHS R01 HL147883NIEHS NIH HHS R01 ES016959NIEHS NIH HHS R01 ES029395NIEHS NIH HHS R01 ES032806NIEHS NIH HHS R01 ES033703NIEHS NIH HHS R56 ES016959NIEHS NIH HHS T32 ES015457
6 · The paper itself

Abstract

Air pollution is a prominent cause of cardiopulmonary illness, but uncertainties remain regarding the mechanisms mediating those effects as well as individual susceptibility. Macrophages are highly responsive to particles, and we hypothesized that their responses would be dependent on their genetic backgrounds. We conducted a genome-wide analysis of peritoneal macrophages harvested from 24 inbred strains of mice from the Hybrid Mouse Diversity Panel (HMDP). Cells were treated with a DEP methanol extract (DEPe) to elucidate potential pathways that mediate acute responses to air pollution exposures. This analysis showed that 1247 genes were upregulated and 1383 genes were downregulated with DEPe treatment across strains. Pathway analysis identified oxidative stress responses among the most prominent upregulated pathways; indeed, many of the upregulated genes included antioxidants such as Hmox1, Txnrd1, Srxn1, and Gclm, with NRF2 (official gene symbol: Nfe2l2) being the most significant driver. DEPe induced a Mox-like transcriptomic profile, a macrophage subtype typically induced by oxidized phospholipids and likely dependent on NRF2 expression. Analysis of individual strains revealed consistency of overall responses to DEPe and yet differences in the degree of Mox-like polarization across the various strains, indicating DEPe × genetic interactions. These results suggest a role for macrophage polarization in the cardiopulmonary toxicity induced by air pollution.

Indexed as

Air PollutantsTranscriptomeVehicle EmissionsAnimalsMacrophagesMacrophages, PeritonealMiceNF-E2-Related Factor 2Oxidative StressParticulate MatterAir PollutantsNF-E2-Related Factor 2Particulate MatterVehicle EmissionsAir pollutionDiesel exhaust particlesHeme oxygenaseMacrophageNrf2Oxidative stress

Identifiers

PMID38908672
PMCPMC13456106

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.