Evidence map›Paper›PMID 25150279›Full record

ArticleThe Journal of pharmacology and experimental therapeutics2014

Differential effects of complement activation products c3a and c5a on cardiovascular function in hypertensive pregnant rats.

Kathryn E Lillegard, Alex C Loeks-Johnson, Jonathan W Opacich, Jenna M Peterson, Ashley J Bauer, Barbara J Elmquist, Ronald R Regal, Jeffrey S Gilbert, Jean F Regal

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

Article in The Journal of pharmacology and experimental therapeutics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 8% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

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  13. Role of B1 and B2 lymphocytes in placental ischemia-induced hypertension.American journal of physiology. Heart and circulatory physiology · 2019
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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 2 institutions in 1 country.

Kathryn E LillegardDepartment of Biomedical Sciences, University of Minnesota Medical School Duluth (K.E.L., A.C.L.-J., J.W.O., J.M.P., A.J.B., B.J.E., J.S.G., J.F.R.) and Department of Mathematics and Statistics, University of Minnesota Duluth (R.R.R.), Duluth, Minnesota.
Alex C Loeks-JohnsonDepartment of Biomedical Sciences, University of Minnesota Medical School Duluth (K.E.L., A.C.L.-J., J.W.O., J.M.P., A.J.B., B.J.E., J.S.G., J.F.R.) and Department of Mathematics and Statistics, University of Minnesota Duluth (R.R.R.), Duluth, Minnesota.
Jonathan W OpacichDepartment of Biomedical Sciences, University of Minnesota Medical School Duluth (K.E.L., A.C.L.-J., J.W.O., J.M.P., A.J.B., B.J.E., J.S.G., J.F.R.) and Department of Mathematics and Statistics, University of Minnesota Duluth (R.R.R.), Duluth, Minnesota.
Jenna M PetersonDepartment of Biomedical Sciences, University of Minnesota Medical School Duluth (K.E.L., A.C.L.-J., J.W.O., J.M.P., A.J.B., B.J.E., J.S.G., J.F.R.) and Department of Mathematics and Statistics, University of Minnesota Duluth (R.R.R.), Duluth, Minnesota.
Ashley J BauerDepartment of Biomedical Sciences, University of Minnesota Medical School Duluth (K.E.L., A.C.L.-J., J.W.O., J.M.P., A.J.B., B.J.E., J.S.G., J.F.R.) and Department of Mathematics and Statistics, University of Minnesota Duluth (R.R.R.), Duluth, Minnesota.
Barbara J ElmquistDepartment of Biomedical Sciences, University of Minnesota Medical School Duluth (K.E.L., A.C.L.-J., J.W.O., J.M.P., A.J.B., B.J.E., J.S.G., J.F.R.) and Department of Mathematics and Statistics, University of Minnesota Duluth (R.R.R.), Duluth, Minnesota.
Ronald R RegalDepartment of Biomedical Sciences, University of Minnesota Medical School Duluth (K.E.L., A.C.L.-J., J.W.O., J.M.P., A.J.B., B.J.E., J.S.G., J.F.R.) and Department of Mathematics and Statistics, University of Minnesota Duluth (R.R.R.), Duluth, Minnesota.
Jeffrey S GilbertDepartment of Biomedical Sciences, University of Minnesota Medical School Duluth (K.E.L., A.C.L.-J., J.W.O., J.M.P., A.J.B., B.J.E., J.S.G., J.F.R.) and Department of Mathematics and Statistics, University of Minnesota Duluth (R.R.R.), Duluth, Minnesota.
Jean F RegalDepartment of Biomedical Sciences, University of Minnesota Medical School Duluth (K.E.L., A.C.L.-J., J.W.O., J.M.P., A.J.B., B.J.E., J.S.G., J.F.R.) and Department of Mathematics and Statistics, University of Minnesota Duluth (R.R.R.), Duluth, Minnesota jregal@d.umn.edu.
University of Minnesota System · USUniversity of Minnesota, Duluth · US

Funding

Complement Activation in Pregnancy and HypertensionR15HL109843 · NHLBI · UNIVERSITY OF MINNESOTA DULUTH · PI REGAL, JEAN F. · 2011 to 2015
$1.3M
Exercise for the Treatment of Hypertension in Pregnancy: Mechanisms and MediatorsR01HL114096 · NHLBI · UNIVERSITY OF OREGON · PI GILBERT, JEFFREY S · 2012 to 2014
$695k
NHLBI NIH HHS R01 HL114096NHLBI NIH HHS R01-HL114096NHLBI NIH HHS R15 HL109843NHLBI NIH HHS R15-HL109843
6 · The paper itself

Abstract

Early-onset pre-eclampsia is characterized by decreased placental perfusion, new-onset hypertension, angiogenic imbalance, and endothelial dysfunction associated with excessive activation of the innate immune complement system. Although our previous studies demonstrated that inhibition of complement activation attenuates placental ischemia-induced hypertension using the rat reduced uterine perfusion pressure (RUPP) model, the important product(s) of complement activation has yet to be identified. We hypothesized that antagonism of receptors for complement activation products C3a and C5a would improve vascular function and attenuate RUPP hypertension. On gestational day (GD) 14, rats underwent sham surgery or vascular clip placement on ovarian arteries and abdominal aorta (RUPP). Rats were treated once daily with the C5a receptor antagonist (C5aRA), PMX51 (acetyl-F-[Orn-P-(D-Cha)-WR]), the C3a receptor antagonist (C3aRA), SB290157 (N(2)-[(2,2-diphenylethoxy)acetyl]-l-arginine), or vehicle from GD 14-18. Both the C3aRA and C5aRA attenuated placental ischemia-induced hypertension without affecting the decreased fetal weight or decreased concentration of free circulating vascular endothelial growth factor (VEGF) also present in this model. The C5aRA, but not the C3aRA, attenuated placental ischemia-induced increase in heart rate and impaired endothelial-dependent relaxation. The C3aRA abrogated the acute pressor response to C3a peptide injection, but it also unexpectedly attenuated the placental ischemia-induced increase in C3a, suggesting nonreceptor-mediated effects. Overall, these results indicate that both C3a and C5a are important products of complement activation that mediate the hypertension regardless of the reduction in free plasma VEGF. The mechanism by which C3a contributes to placental ischemia-induced hypertension appears to be distinct from that of C5a, and management of pregnancy-induced hypertension is likely to require a broad anti-inflammatory approach.

Indexed as

AnimalsCardiovascular SystemComplement ActivationComplement C3aComplement C5aDisease Models, AnimalEndothelium, VascularFemaleHeart RateHypertensionIschemiaPlacentaPregnancyRatsReceptors, ComplementVascular Endothelial Growth Factor AComplement C3aComplement C5aReceptors, ComplementVascular Endothelial Growth Factor A

Identifiers

PMID25150279
PMCPMC4201271
OpenAlexW2058344851

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.