Evidence map›Paper›PMID 38746124›Full record

ArticleResearch square2024

Peroxisome proliferator-activated receptor alpha is essential factor in enhanced macrophage immune function induced by angiotensin converting enzyme.

Suguru Saito, DuoYao Cao, Ellen A Bernstein, Anthony E Jones, Amy Rios, Aoi O Hoshi, Aleksandr B Stotland, Erika E Nishi, Tomohiro Shibata, Faizan Ahmed and 4 more

Abstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in Research square, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors.

Suguru SaitoDepartment of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
DuoYao CaoDepartment of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Ellen A BernsteinDepartment of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Anthony E JonesDepartment of Molecular and Medical Pharmacology, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Amy RiosDepartment of Molecular and Medical Pharmacology, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Aoi O HoshiDepartment of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Aleksandr B StotlandDepartment of Cardiology, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, 90048, USA.
Erika E NishiDepartment of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Tomohiro ShibataDepartment of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Faizan AhmedDivision of Gastroenterology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Jennifer E Van EykDepartment of Cardiology, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, 90048, USA.
Ajit DivakaruniDepartment of Molecular and Medical Pharmacology, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Zakir KhanDepartment of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Kenneth E BernsteinDepartment of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.

Funding

Exosome Therapeutics to Dissect HFpEF MechanismsR01HL155346 · NHLBI · CEDARS-SINAI MEDICAL CENTER · PI MARBAN, EDUARDO, VAN EYK, JENNIFER E · 2021 to 2024
$3.3M
ACE and myeloid cell metabolismR01AI164519 · NIAID · CEDARS-SINAI MEDICAL CENTER · PI KENNETH E BERNSTEIN · 2022 to 2026
$3.1M
NHLBI NIH HHS R01 HL155346NIAID NIH HHS R01 AI164519
6 · The paper itself

Abstract

An upregulation of angiotensin-converting enzyme (ACE) expression strengthens the immune activity of myeloid lineage cells as a natural functional regulation mechanism in our immunity. ACE10/10 mice, possessing increased ACE expression in macrophages, exhibit enhanced anti-tumor immunity and anti-bactericidal effects compared to those of wild type (WT) mice, while the detailed molecular mechanism has not been elucidated yet. In this report, we demonstrate that peroxisome proliferator-activated receptor alpha (PPARα) is a key molecule in the functional upregulation of macrophages induced by ACE. The expression of PPARα, a transcription factor regulating fatty acid metabolism-associated gene expressions, was upregulated in ACE-overexpressing macrophages. To pinpoint the role of PPARα in the enhanced immune function of ACE-overexpressing macrophages, we established a line with myeloid lineage-selective PPARα depletion employing the Lysozyme 2 (LysM)-Cre system based on ACE 10/10 mice (named A10-PPARα-Cre). Interestingly, A10-PPARα-Cre mice exhibited larger B16-F10-originated tumors than original ACE 10/10 mice. PPARα depletion impaired cytokine production and antigen-presenting activity in ACE-overexpressing macrophages, resulting in reduced tumor antigen-specific CD8+ T cell activity. Additionally, the anti-bactericidal effect was also impaired in A10-PPARα-Cre mice, resulting in similar bacterial colonization to WT mice in Methicillin-Resistant

Indexed as

angiotensin converting enzymeanti-tumor immunitybacterial clearancemacrophagesPPARα

Identifiers

PMID38746124
PMCPMC11092867

What Socratic holds

Textmetadata
LicenceCC BY
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.