Evidence map›Paper›PMID 26831193›Full record

ArticleHypertension (Dallas, Tex. : 1979)2016

Placental Growth Factor Administration Abolishes Placental Ischemia-Induced Hypertension.

Frank T Spradley, Adelene Y Tan, Woo S Joo, Garrett Daniels, Paul Kussie, S Ananth Karumanchi, Joey P Granger

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

Article in Hypertension (Dallas, Tex. : 1979), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 1 pooled it
21.8field-weighted citation impact, top 1% 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

71 citing papers in PubMed, 1 synthesis or guideline pooled it, 143 citations in OpenAlex.

  1. Pooled it
  2. Transforming Preeclampsia Care: Molecular Diagnostics and Therapeutic Innovations.Journal of the American Society of Nephrology : JASN · 2026
    Review
  3. Review
  4. Therapeutic Interventions for Preeclampsia: Integrating Placental and Maternal Perspectives.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026
    Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. VASCULAR AND RENAL MECHANISMS OF PREECLAMPSIA.Current opinion in physiology · 2023
    Article
  18. Article
  19. Review
  20. Review

11 more citing papers are in PubMed but not listed here.

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 at 1 institution in 1 country.

Frank T SpradleyFrom the Department of Surgery (F.T.S.), Department of Physiology and Biophysics (F.T.S., J.P.G.), and Cardiovascular-Renal Research Center (F.T.S., J.P.G.), The University of Mississippi Medical Center, Jackson; Aggamin Biologics, New York, NY (A.Y.T., W.S.J., G.D., P.K.); and Beth Israel Deaconess Medical Center, Department of Nephrology, Harvard Medical School, Boston, MA (S.A.K.). jgranger@umc.edu fspradley@umc.edu.
Adelene Y TanFrom the Department of Surgery (F.T.S.), Department of Physiology and Biophysics (F.T.S., J.P.G.), and Cardiovascular-Renal Research Center (F.T.S., J.P.G.), The University of Mississippi Medical Center, Jackson; Aggamin Biologics, New York, NY (A.Y.T., W.S.J., G.D., P.K.); and Beth Israel Deaconess Medical Center, Department of Nephrology, Harvard Medical School, Boston, MA (S.A.K.).
Woo S JooFrom the Department of Surgery (F.T.S.), Department of Physiology and Biophysics (F.T.S., J.P.G.), and Cardiovascular-Renal Research Center (F.T.S., J.P.G.), The University of Mississippi Medical Center, Jackson; Aggamin Biologics, New York, NY (A.Y.T., W.S.J., G.D., P.K.); and Beth Israel Deaconess Medical Center, Department of Nephrology, Harvard Medical School, Boston, MA (S.A.K.).
Garrett DanielsFrom the Department of Surgery (F.T.S.), Department of Physiology and Biophysics (F.T.S., J.P.G.), and Cardiovascular-Renal Research Center (F.T.S., J.P.G.), The University of Mississippi Medical Center, Jackson; Aggamin Biologics, New York, NY (A.Y.T., W.S.J., G.D., P.K.); and Beth Israel Deaconess Medical Center, Department of Nephrology, Harvard Medical School, Boston, MA (S.A.K.).
Paul KussieFrom the Department of Surgery (F.T.S.), Department of Physiology and Biophysics (F.T.S., J.P.G.), and Cardiovascular-Renal Research Center (F.T.S., J.P.G.), The University of Mississippi Medical Center, Jackson; Aggamin Biologics, New York, NY (A.Y.T., W.S.J., G.D., P.K.); and Beth Israel Deaconess Medical Center, Department of Nephrology, Harvard Medical School, Boston, MA (S.A.K.).
S Ananth KarumanchiFrom the Department of Surgery (F.T.S.), Department of Physiology and Biophysics (F.T.S., J.P.G.), and Cardiovascular-Renal Research Center (F.T.S., J.P.G.), The University of Mississippi Medical Center, Jackson; Aggamin Biologics, New York, NY (A.Y.T., W.S.J., G.D., P.K.); and Beth Israel Deaconess Medical Center, Department of Nephrology, Harvard Medical School, Boston, MA (S.A.K.).
Joey P GrangerFrom the Department of Surgery (F.T.S.), Department of Physiology and Biophysics (F.T.S., J.P.G.), and Cardiovascular-Renal Research Center (F.T.S., J.P.G.), The University of Mississippi Medical Center, Jackson; Aggamin Biologics, New York, NY (A.Y.T., W.S.J., G.D., P.K.); and Beth Israel Deaconess Medical Center, Department of Nephrology, Harvard Medical School, Boston, MA (S.A.K.). jgranger@umc.edu fspradley@umc.edu.
Aggamin (United States) · US

Funding

STRUCTURAL VASCULAR ADAPTATION OF THE MICROCIRCULATIONP01HL051971 · NHLBI · UNIVERSITY OF MISSISSIPPI MEDICAL CENTER · PI HESTER, ROBERT L · 1993 to 2018
$39.4M
The role of leptin in autoimmune-associated hypertensionP20GM104357 · NIGMS · UNIVERSITY OF MISSISSIPPI MED CTR · PI TAYLOR, ERIN BASSFORD · 2013 to 2022
$23.4M
Hypertension and Cardiorenal Research Training ProgramT32HL105324 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI Joey P. Granger · 2010 to 2026
$7.8M
Hypertension, Kidney and PregnancyR01HL108618 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI GRANGER, JOEY P. · 2011 to 2015
$1.8M
Development of a Novel Biologic to Treat PreeclampsiaR43HD082657 · NICHD · AGGAMIN PHARMACEUTICALS, LLC · PI TAN, ADELENE · 2014 to 2014
$218k
NHLBI NIH HHS P01 HL051971NHLBI NIH HHS R01 HL108618NHLBI NIH HHS T32 HL105324NHLBI NIH HHS T32HL105324-01NICHD NIH HHS R43 HD082657NICHD NIH HHS SBIR 1R43HD082657NIGMS NIH HHS P20 GM104357
6 · The paper itself

Abstract

Preeclampsia is a pregnancy-specific disorder of new-onset hypertension. Unfortunately, the most effective treatment is early delivery of the fetus and placenta. Placental ischemia appears central to the pathogenesis of preeclampsia because placental ischemia/hypoxia induced in animals by reduced uterine perfusion pressure (RUPP) or in humans stimulates release of hypertensive placental factors into the maternal circulation. The anti-angiogenic factor soluble fms-like tyrosine kinase-1 (sFlt-1), which antagonizes and reduces bioavailable vascular endothelial growth factor and placental growth factor (PlGF), is elevated in RUPP rats and preeclampsia. Although PlGF and vascular endothelial growth factor are both natural ligands for sFlt-1, vascular endothelial growth factor also has high affinity to VEGFR2 (Flk-1) causing side effects like edema. PlGF is specific for sFlt-1. We tested the hypothesis that PlGF treatment reduces placental ischemia-induced hypertension by antagonizing sFlt-1 without adverse consequences to the mother or fetus. On gestational day 14, rats were randomized to 4 groups: normal pregnant or RUPP±infusion of recombinant human PlGF (180 μg/kg per day; AG31, a purified, recombinant human form of PlGF) for 5 days via intraperitoneal osmotic minipumps. On day 19, mean arterial blood pressure and plasma sFlt-1 were higher and glomerular filtration rate lower in RUPP than normal pregnant rats. Infusion of recombinant human PlGF abolished these changes seen with RUPP along with reducing oxidative stress. These data indicate that the increased sFlt-1 and reduced PlGF resulting from placental ischemia contribute to maternal hypertension. Our novel finding that recombinant human PlGF abolishes placental ischemia-induced hypertension, without major adverse consequences, suggests a strong therapeutic potential for this growth factor in preeclampsia.

Indexed as

Pregnancy, AnimalAnalysis of VarianceAnimalsEnzyme-Linked Immunosorbent AssayFemaleHumansHypertension, Pregnancy-InducedIschemiaOxidative StressPlacentaPlacenta Growth FactorPlacental CirculationPlacental InsufficiencyPre-EclampsiaPregnancyPregnancy ProteinsPGF protein, humanPgf protein, ratPlacenta Growth FactorPregnancy Proteinsblood pressurepreeclampsiapregnancyratRUPP

Identifiers

PMID26831193
PMCPMC4786447
OpenAlexW2267669237

What OpenQuestion 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 OpenQuestion graph.