Evidence map›Paper›PMID 24763822›Full record

ArticlePloS one2014

Loss of function of endothelin-2 leads to reduced ovulation and CL formation.

Joseph A Cacioppo, Sang Wook Oh, Hey-young Kim, Jongki Cho, Po-Ching Patrick Lin, Masashi Yanagisawa, CheMyong Ko

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
4.4field-weighted citation impact, top 6% 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

16 citing papers in PubMed, 36 citations in OpenAlex.

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  14. In vivo imaging reveals an essential role of vasoconstriction in rupture of the ovarian follicle at ovulation.Proceedings of the National Academy of Sciences of the United States of America · 2016
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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

7 authors at 2 institutions in 2 countries.

Joseph A CacioppoComparative Biosciences, College of Veterinary Medicine, University of Illinois, Urbana-Champaign, Illinois, United States of America.
Sang Wook OhComparative Biosciences, College of Veterinary Medicine, University of Illinois, Urbana-Champaign, Illinois, United States of America; Department of Biology Education, Institute of Fusion Science, Chonbuk National University, Jeonju, South Korea.
Hey-young KimComparative Biosciences, College of Veterinary Medicine, University of Illinois, Urbana-Champaign, Illinois, United States of America.
Jongki ChoComparative Biosciences, College of Veterinary Medicine, University of Illinois, Urbana-Champaign, Illinois, United States of America; College of Veterinary Medicine, Research Institute of Veterinary Medicine, Chungnam National University, Daejon, South Korea.
Po-Ching Patrick LinComparative Biosciences, College of Veterinary Medicine, University of Illinois, Urbana-Champaign, Illinois, United States of America.
Masashi YanagisawaHoward Hughes Medical Institute and Departments of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas, Texas, United States of America.
CheMyong KoComparative Biosciences, College of Veterinary Medicine, University of Illinois, Urbana-Champaign, Illinois, United States of America.
University of Illinois Urbana-Champaign · USThe University of Texas Southwestern Medical Center · US

Funding

Endothelin-2 in Ovarian Follicle RuptureR01HD052694 · NICHD · UNIVERSITY OF KENTUCKY · PI CURRY, THOMAS E · 2006 to 2010
$1.2M
NICHD NIH HHS R01 HD052694NICHD NIH HHS R01HD052694
6 · The paper itself

Abstract

Endothelin-2 (EDN2), a potent vasoconstrictive peptide, is transiently produced by periovulatory follicles at the time of ovulation when corpus luteum (CL) formation begins. EDN2 induces contraction of ovarian smooth muscles ex vivo via an endothelin receptor A-mediated pathway. In this study, we aimed to determine if EDN2 is required for normal ovulation and subsequent CL formation in?vivo. In the ovaries of a mouse model that globally lacks the Edn2 gene (Edn2 knockout mouse; Edn2KO), histology showed that post-pubertal Edn2KO mice possess follicles of all developmental stages, but no corpora lutea. When exogenous gonadotropins were injected to induce super-ovulation, Edn2KO mice exhibited significantly impaired ovulation and CL formation compared to control littermates. Edn2KO ovaries that did ovulate in response to gonadotropins did not contain histologically and functionally identifiable CL. Intra-ovarian injection of EDN2 peptide results suggest partial induction of ovulation in Edn2KO mice. Endothelin receptor antagonism in wild type mice similarly disrupted ovulation, CL formation, and progesterone secretion. Overall, this study suggests that EDN2 is necessary for normal ovulation and CL formation.

Indexed as

AnimalsCorpus LuteumEndothelin-2Endothelin Receptor AntagonistsFemaleGonadotropinsMice, Inbred C57BLMice, KnockoutNeovascularization, PhysiologicOvarian FollicleOvulationEndothelin-2Endothelin Receptor AntagonistsGonadotropins

Identifiers

PMID24763822
PMCPMC3999112
OpenAlexW2021574248

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.