Evidence map›Paper›PMID 31138432›Full record

ArticlePlacenta2019

Aldehyde dehydrogenase isoforms and inflammatory cell populations are differentially expressed in term human placentas affected by intrauterine growth restriction.

Alison Chu, Parisa Najafzadeh, Peggy Sullivan, Brian Cone, Ryan Elshimali, Hania Shakeri, Carla Janzen, Vei Mah, Madhuri Wadehra

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

Article in Placenta, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

12 citing papers in PubMed, 19 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

9 authors at 1 institution in 1 country.

Alison ChuDepartment of Pediatrics, Division of Neonatology and Developmental Biology, David Geffen School of Medicine at UCLA, 10833 LeConte Avenue, Room B2-375 MDCC, Los Angeles, CA, 90095, USA. Electronic address: alisonchu@mednet.ucla.edu.
Parisa NajafzadehDepartment of Pathology and Laboratory Medicine, 4525 MacDonald Research Laboratories, Geffen School of Medicine at UCLA, Los Angeles, CA, 90095, USA. Electronic address: najafzadehparisa@gmail.com.
Peggy SullivanDepartment of Pathology and Laboratory Medicine, 4525 MacDonald Research Laboratories, Geffen School of Medicine at UCLA, Los Angeles, CA, 90095, USA. Electronic address: psullivan@mednet.ucla.edu.
Brian ConeDepartment of Pathology and Laboratory Medicine, 4525 MacDonald Research Laboratories, Geffen School of Medicine at UCLA, Los Angeles, CA, 90095, USA.
Ryan ElshimaliDepartment of Pathology and Laboratory Medicine, 4525 MacDonald Research Laboratories, Geffen School of Medicine at UCLA, Los Angeles, CA, 90095, USA. Electronic address: ryanelshimali@gmail.com.
Hania ShakeriDepartment of Pathology and Laboratory Medicine, 4525 MacDonald Research Laboratories, Geffen School of Medicine at UCLA, Los Angeles, CA, 90095, USA. Electronic address: hania.shakeri@gmail.com.
Carla JanzenDepartment of Obstetrics and Gynecology, David Geffen School of Medicine at UCLA, 10833 Le Conte Avenue, Room 22-172, Los Angeles, CA, 90095, USA. Electronic address: cjanzen@mednet.ucla.edu.
Vei MahDepartment of Pathology and Laboratory Medicine, 4525 MacDonald Research Laboratories, Geffen School of Medicine at UCLA, Los Angeles, CA, 90095, USA. Electronic address: vei.mah@gmail.com.
Madhuri WadehraDepartment of Pathology and Laboratory Medicine, 4525 MacDonald Research Laboratories, Geffen School of Medicine at UCLA, Los Angeles, CA, 90095, USA; Jonsson Comprehensive Cancer Center, David Geffen School of Medicine at UCLA, 8-684 Factor Building, Los Angeles, CA, 90095, USA; Center to Eliminate Cancer Health Disparities, Charles Drew University, 1731 East 120th Street, Los Angeles, CA, 90059, USA. Electronic address: mwadehra@mednet.ucla.edu.
University of California, Los Angeles · US

Funding

The Effect of Nanoparticle Encapsulated Resveratrol on Treatment of PeriodontitisKL2TR001882 · NCATS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Elizabeta Nemeth · 2016 to 2026
$13.1M
Using EMP2 for Image Guided Drug Delivery for Breast CancerR01CA163971 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI OLAFSEN, TOVE, WADEHRA, MADHURI · 2012 to 2016
$1.6M
The role of IL10 in early vascularity, endothelial dysfunction, and programming of adult cardiovascular diseaseK08HD093874 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CHU, ALISON · 2018 to 2020
$536k
NCATS NIH HHS KL2 TR001882NCI NIH HHS R01 CA163971NICHD NIH HHS K08 HD093874
6 · The paper itself

Abstract

objectiveIntrauterine growth restriction (IUGR) is a complication of pregnancy that has both short- and long-term sequelae for affected mothers and offspring. The pathophysiology of disease stems from poor nutrient and oxygen provision to the fetus, resulting in increased oxidative stress within the placenta. As the milieu within the local microenvironment alters macrophage differentiation, we hypothesized that macrophage plasticity may be altered in placentas associated with IUGR, and that macrophages would show hallmarks of lipid peroxidation including altered aldehyde metabolism.

methodsIn human placentas taken from normal pregnancies resulting in appropriate-for-gestational-age (AGA) newborns and placentas associated with IUGR, placental macrophages were evaluated by immunohistochemistry and shown in IUGR to resemble pro-inflammatory activated M1-type macrophages. To link oxidative stress to macrophages, the expression of aldehyde dehydrogenase (ALDHs) isozymes ALDH1, ALDH2, and ALDH3 was assessed.

resultsAll three isozymes displayed preferential staining for distinct cellular populations within the term human placenta. ALDH1 and ALDH2 were strongly expressed in placental Hofbauer and decidual stromal cells. ALDH3, in contrast, was present in extravillous trophoblasts. Comparing AGA and IUGR-associated placentas, ALDH1 and ALDH2 trended to have greater expression in macrophage populations but lower expression in decidual cell populations in IUGR-associated placentas. ALDH3 had higher expression in IUGR-associated placentas but localized specifically to extravillous trophoblast populations.

conclusionTherefore, we speculate that specific ALDH isozymes have cell-specific functions related to differentiation, inflammation, or oxidative stress responses that are altered in IUGR-associated term human placentas. This family of isozymes may be a novel method to identify human placentas affected by placental insufficiency/IUGR.

Indexed as

AdultAldehyde DehydrogenaseFemaleFetal Growth RetardationHumansMacrophagesPlacentaPregnancyProtein IsoformsAldehyde DehydrogenaseProtein IsoformsAldehyde dehydrogenase (ALDH)Intrauterine growth restrictionMacrophage polarizationOxidative stressPlacentaPlacental insufficiency

Identifiers

PMID31138432
PMCPMC6719708
OpenAlexW2939338670

What OpenQuestion holds

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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.