Evidence map›Paper›PMID 28241318›Full record

ArticleInvestigative ophthalmology & visual science2017

The Nicotinic Cholinergic Pathway Contributes to Retinal Neovascularization in a Mouse Model of Retinopathy of Prematurity.

Sean F Hackett, Christopher Seidel, Sheena Abraham, Rishi Chadha, Seth D Fortmann, Peter A Campochiaro, John P Cooke

Abstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

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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.

Sean F HackettWilmer Eye Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland, United States.
Christopher SeidelWilmer Eye Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland, United States.
Sheena AbrahamDivision of Cardiovascular Medicine, Stanford University, Stanford, California, United States.
Rishi ChadhaWilmer Eye Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland, United States.
Seth D FortmannWilmer Eye Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland, United States.
Peter A CampochiaroWilmer Eye Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland, United States.
John P CookeDepartment of Cardiovascular Sciences, Methodist Hospital System, Houston, Texas, United States.

Funding

Basic and Translational Research iPSC-based hematologic and vascular therapiesU01HL100397 · NHLBI · STANFORD UNIVERSITY · PI COOKE, JOHN P · 2009 to 2015
$7.4M
NHLBI NIH HHS U01 HL100397
6 · The paper itself

Abstract

Purpose: To investigate the role of nicotinic acetylcholine receptors (nAChRs) in retinal vascular development and ischemia-induced retinal neovascularization (NV). Methods: The expression of nAChR subtypes and VEGF signaling pathway components was assessed in mice with and without oxygen-induced ischemic retinopathy by comparing expression levels at postnatal day (P) 14 and P17 in mice exposed to 75% oxygen from P7 to P12 and returned to room air versus mice pups that were exposed to ambient oxygen levels during the same period. The effect of topical or intraocular injection of mecamylamine, a nonspecific nAChR antagonist, or targeted deletion of α7- or α9-nAChRs on ischemia-induced retinal NV was determined by comparing the amount of retinal NV at P17 in these mice versus appropriate controls. Results: The expression of nAChR subunits and components of the VEGF signaling pathways was increased in ischemic retina. Topical application or intraocular injection of mecamylamine decreased retinal NV in this model. Mecamylamine had no effect on normal retinal vascular development or on revascularization of the central retinal area of nonperfusion in mice with ischemic retinopathy. Targeted deletion of α9, but not α7, nAChR receptor subunits reduced retinal NV in mice with ischemic retinopathy. Conclusion: These data suggest that nAChR signaling, primarily through the α9 nAChR subunit, contributes to ischemia-induced retinal NV, but not retinal vascular development. Mecamylamine or a specific α9 nAChR antagonist could be considered for treatment of retinopathy of prematurity and other ischemic retinopathies.

Indexed as

AnimalsAnimals, NewbornCholinergic AgentsDisease Models, AnimalIschemiaMecamylamineMiceMice, Inbred C57BLNeovascularization, PathologicNicotinic AntagonistsProtein SubunitsReceptors, NicotinicRetinaRetinal NeovascularizationRetinal VesselsRetinopathy of PrematurityCholinergic AgentsMecamylamineNicotinic AntagonistsProtein SubunitsReceptors, NicotinicVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2

Identifiers

PMID28241318
PMCPMC6020715

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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.