Evidence map›Paper›PMID 32385775›Full record

ArticleAngiogenesis2020

Endothelial deletion of ADAM10, a key regulator of Notch signaling, causes impaired decidualization and reduced fertility in female mice.

Nicole Lustgarten Guahmich, Gregory Farber, Shiva Shafiei, Dylan McNally, David Redmond, Eleni Kallinos, Heidi Stuhlmann, Daniel Dufort, Daylon James, Carl P Blobel

Open access · greenAbstract read
In one paragraph

Article in Angiogenesis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Signaling via retinoic acid receptors mediates decidual angiogenesis in mice and human stromal cell decidualization.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
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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

10 authors at 3 institutions in 2 countries.

Nicole Lustgarten GuahmichDepartment of Physiology, Biophysics and Systems Biology, Weill Cornell Medicine, New York, NY, USA.
Gregory FarberDepartment of Physiology, Biophysics and Systems Biology, Weill Cornell Medicine, New York, NY, USA.
Shiva ShafieiResearch Institute of the McGill University Health Centre, Montréal, QC, Canada.
Dylan McNallyDepartment of Physiology, Biophysics and Systems Biology, Weill Cornell Medicine, New York, NY, USA.
David RedmondCenter for Reproductive Medicine and Infertility, Weill Cornell Medicine, New York, NY, USA.
Eleni KallinosCenter for Reproductive Medicine and Infertility, Weill Cornell Medicine, New York, NY, USA.
Heidi StuhlmannDepartment of Cell and Developmental Biology, Weill Cornell Medicine, New York, NY, USA.
Daniel DufortResearch Institute of the McGill University Health Centre, Montréal, QC, Canada.
Daylon JamesCenter for Reproductive Medicine and Infertility, Weill Cornell Medicine, New York, NY, USA.
Carl P BlobelDepartment of Physiology, Biophysics and Systems Biology, Weill Cornell Medicine, New York, NY, USA. blobelc@hss.edu.ORCID 0000-0001-5053-3137
Cornell University · USMcGill University Health Centre · CAHospital for Special Surgery · US

Funding

Testosterone-GnRH Frequency and the Evolution of PCOS in AdolescenceP50HD028934 · NICHD · UNIVERSITY OF VIRGINIA · PI HAISENLEDER, DANIEL J. · 2014 to 2018
$8.6M
iRhoms 1 and 2: Key regulators of ADAM17-dependent EGFR signalingR01GM064750 · NIGMS · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI BLOBEL, CARL PETER · 2002 to 2019
$6.1M
Role of Egfl7 in Vascular Development and AngiogenesisR01HL082098 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI STUHLMANN, HEIDI · 2006 to 2015
$3.3M
Role of iRhoms and ADAM17 in EGFR and TNFalpha signalingR35GM134907 · NIGMS · HOSPITAL FOR SPECIAL SURGERY · PI BLOBEL, CARL PETER · 2020 to 2024
$2.0M
Eunice Kennedy Shriver National Institute of Child Health and Human Development P50-HD28934NHLBI NIH HHS R01 HL082098NICHD NIH HHS P50 HD028934NIGMS NIH HHS R01 GM064750NIGMS NIH HHS R35 GM134907
6 · The paper itself

Abstract

During the initiation of pregnancy, the vasculature of the implantation site expands rapidly, yet little is known about this process or its role in fertility. Here, we report that endothelial-specific deletion of a disintegrin and metalloprotease 10 (ADAM10), an essential regulator of Notch signaling, results in severe subfertility in mice. We found that implantation sites develop until 5.5 days post conception (dpc) but are resorbed by 6.5 dpc in A10ΔEC mice. Analysis of the mutant implantation sites showed impaired decidualization and abnormal vascular patterning compared to controls. Moreover, RNA-seq analysis revealed changes in endothelial cell marker expression consistent with defective ADAM10/Notch signaling in samples from A10ΔEC mice, suggesting that this signaling pathways is essential for the physiological function of endometrial endothelial cells during early pregnancy. Our findings raise the possibility that impaired endothelial cell function could be a cause for repeated pregnancy loss (RPL) and infertility in humans.

Indexed as

FertilityGene DeletionSignal TransductionADAM10 ProteinAmyloid Precursor Protein SecretasesAnimalsDeciduaFemaleMembrane ProteinsMiceMice, KnockoutPregnancyReceptors, NotchADAM10 ProteinAdam10 protein, mouseAmyloid Precursor Protein SecretasesMembrane ProteinsReceptors, NotchADAM10 (a disintegrin and metalloprotease 10)Endometrial vasculatureEndothelial cellsInfertilityNotch

Identifiers

PMID32385775
PMCPMC8603441
OpenAlexW3022668259

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.