Evidence map›Paper›PMID 40037635›Full record

ArticleEndocrinology2025

Neurotensin Regulates Primate Ovulation Via Multiple Neurotensin Receptors.

Andrew C Pearson, Jessica S Miller, Hannah J Jensen, Ketan Shrestha, Thomas E Curry, Diane M Duffy

Abstract read
In one paragraph

Article in Endocrinology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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.

Andrew C PearsonDepartment of Basic and Translational Sciences, Eastern Virginia Medical School, Old Dominion University, Norfolk, VA 23501, USA.
Jessica S MillerDepartment of Basic and Translational Sciences, Eastern Virginia Medical School, Old Dominion University, Norfolk, VA 23501, USA.
Hannah J JensenDepartment of Basic and Translational Sciences, Eastern Virginia Medical School, Old Dominion University, Norfolk, VA 23501, USA.
Ketan ShresthaDepartment of Obstetrics and Gynecology, University of Kentucky, Lexington, KY 40506, USA.
Thomas E CurryDepartment of Obstetrics and Gynecology, University of Kentucky, Lexington, KY 40506, USA.
Diane M DuffyDepartment of Basic and Translational Sciences, Eastern Virginia Medical School, Old Dominion University, Norfolk, VA 23501, USA.ORCID 0000-0001-9345-2740

Funding

Neurotensin: A Novel Mediator of OvulationR01HD097675 · NICHD · UNIVERSITY OF KENTUCKY · PI CURRY, THOMAS E, DUFFY, DIANE M · 2019 to 2023
$3.3M
Eunice Kennedy Shriver National Institute of Child Health and Human Development HD097675NICHD NIH HHS R01 HD097675
6 · The paper itself

Abstract

Neurotensin (NTS), a small neuropeptide, was recently established as a key paracrine mediator of ovulation. NTS mRNA is highly expressed by granulosa cells in response to the luteinizing hormone surge, and multiple NTS receptors are expressed by cells of the ovulatory follicle. To identify the role of NTS receptors NTSR1 and SORT1 in ovulation in vivo, the dominant follicle of cynomolgus macaques (Macaca fascicularis) was injected with either vehicle control, the general NTS receptor antagonist SR142948, the NTSR1-selective antagonist SR48692, or the SORT1-selective antagonist AF38469. hCG was then administered to initiate ovulatory events. Ovulation was successful in all control-injected follicles. Rupture sites were smaller or absent after injection with NTS receptor antagonists. Histological analysis of follicles injected with SR142948, SR48692, or AF38469 revealed increased red blood cell extravasation and pooling in the follicle antrum when compared to controls. NTS receptor antagonist-injected follicles also showed dysregulated capillary formation and reduced luteinization of the granulosa cell layer. Prior in vitro studies showed that NTS significantly increased monkey ovarian microvascular endothelial cell (mOMEC) migration, while decreasing monolayer permeability. The NSTR1 antagonist SR48692 or siRNA knockdown of NTSR1 abrogated the ability of NTS to stimulate mOMEC migration and to decrease monolayer permeability. Similar experiments performed with the SORT1 antagonist AF38469 or siRNA knockdown of SORT1 also resulted in ablation of NTS-mediated changes in migration and permeability after SORT1 signaling was impaired. Together, these data implicate both NTSR1 and SORT1 to be critical mediators of NTS-stimulated ovulation, luteinization, and angiogenesis of the ovulatory follicle.

Indexed as

NeurotensinOvulationReceptors, NeurotensinAnimalsChorionic GonadotropinFemaleGranulosa CellsMacaca fascicularisOvarian FolliclePyrazolesQuinolinesChorionic GonadotropinNeurotensinneurotensin type 1 receptorPyrazolesQuinolinesReceptors, NeurotensinSR 48692angiogenesisendothelial cellluteinizationmonkeyovarysortilin

Identifiers

PMID40037635
PMCPMC11979100

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Registered trials

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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.