Evidence map›Paper›PMID 26135305›Full record

ArticlePloS one2015

Neutrophil Depletion Attenuates Placental Ischemia-Induced Hypertension in the Rat.

Jean F Regal, Kathryn E Lillegard, Ashley J Bauer, Barbara J Elmquist, Alex C Loeks-Johnson, Jeffrey S Gilbert

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.0field-weighted citation impact, top 7% 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

33 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
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  12. Neutrophils Mediate Pulmonary Artery Thrombosis In Situ.International journal of molecular sciences · 2022
    Article
  13. Review
  14. Article
  15. Review
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  17. Article
  18. Vascular mechanisms and molecular targets in hypertensive pregnancy and preeclampsia.American journal of physiology. Heart and circulatory physiology · 2020
    Review
  19. Review
  20. Review
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

6 authors at 1 institution in 1 country.

Jean F RegalDepartment of Biomedical Sciences, University of Minnesota Medical School Duluth, Duluth, Minnesota, United States of America.
Kathryn E LillegardDepartment of Biomedical Sciences, University of Minnesota Medical School Duluth, Duluth, Minnesota, United States of America.
Ashley J BauerDepartment of Biomedical Sciences, University of Minnesota Medical School Duluth, Duluth, Minnesota, United States of America.
Barbara J ElmquistDepartment of Biomedical Sciences, University of Minnesota Medical School Duluth, Duluth, Minnesota, United States of America.
Alex C Loeks-JohnsonDepartment of Biomedical Sciences, University of Minnesota Medical School Duluth, Duluth, Minnesota, United States of America.
Jeffrey S GilbertDepartment of Biomedical Sciences, University of Minnesota Medical School Duluth, Duluth, Minnesota, United States of America.
University of Minnesota, Duluth · US

Funding

Pathway to Advanced Degrees in Life SciencesR25GM086669 · NIGMS · UNIVERSITY OF MINNESOTA DULUTH · PI ANDERSON, GRANT W, CLARKE, BENJAMIN L · 2009 to 2017
$2.8M
Complement Activation in Pregnancy and HypertensionR15HL109843 · NHLBI · UNIVERSITY OF MINNESOTA DULUTH · PI REGAL, JEAN F. · 2011 to 2015
$1.3M
NHLBI NIH HHS R15 HL109843NIGMS NIH HHS R25 GM086669
6 · The paper itself

Abstract

Preeclampsia is characterized by reduced placental perfusion with placental ischemia and hypertension during pregnancy. Preeclamptic women also exhibit a heightened inflammatory state and greater number of neutrophils in the vasculature compared to normal pregnancy. Since neutrophils are associated with tissue injury and inflammation, we hypothesized that neutrophils are critical to placental ischemia-induced hypertension and fetal demise. Using the reduced uteroplacental perfusion pressure (RUPP) model of placental ischemia-induced hypertension in the rat, we determined the effect of neutrophil depletion on blood pressure and fetal resorptions. Neutrophils were depleted with repeated injections of polyclonal rabbit anti-rat polymorphonuclear leukocyte (PMN) antibody (antiPMN). Rats received either antiPMN or normal rabbit serum (Control) on 13.5, 15.5, 17.5, and 18.5 days post conception (dpc). On 14.5 dpc, rats underwent either Sham surgery or clip placement on ovarian arteries and abdominal aorta to reduce uterine perfusion pressure (RUPP). On 18.5 dpc, carotid arterial catheters were placed and mean arterial pressure (MAP) was measured on 19.5 dpc. Neutrophil-depleted rats had reduced circulating neutrophils from 14.5 to 19.5 dpc compared to Control, as well as decreased neutrophils in lung and placenta on 19.5 dpc. MAP increased in RUPP Control vs Sham Control rats, and neutrophil depletion attenuated this increase in MAP in RUPP rats without any effect on Sham rats. The RUPP-induced increase in fetal resorptions and complement activation product C3a were not affected by neutrophil depletion. Thus, these data are the first to indicate that neutrophils play an important role in RUPP hypertension and that cells of the innate immune system may significantly contribute to pregnancy-induced hypertension.

Indexed as

Leukocyte Reduction ProceduresAnimalsComplement C3aDisease Models, AnimalFemaleHypertension, Pregnancy-InducedImmune SeraImmunity, InnateIschemiaLeukocyte CountNeutrophilsOxidative StressPlacentaPlacental CirculationPre-EclampsiaPregnancyComplement C3aImmune SeraVascular Endothelial Growth Factor Avascular endothelial growth factor A, rat

Identifiers

PMID26135305
PMCPMC4509576
OpenAlexW785245612

What OpenQuestion 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 OpenQuestion graph.