Evidence map›Paper›PMID 42134448›Full record

ArticleExperimental eye research2026

A human amelotin transgenic mouse model with calcified deposits similar to those in dry age-related macular degeneration.

Dinusha Rajapakse, Jianguo Fan, Dannika Daily, Lijin Dong, Katherine Peterson, Robert Fariss, Graeme Wistow

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Experimental eye research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Dinusha RajapakseSection on Molecular Structure and Functional Genomics, National Institutes of Health, National Eye Institute, Bethesda, MD, 20892, United States.
Jianguo FanSection on Molecular Structure and Functional Genomics, National Institutes of Health, National Eye Institute, Bethesda, MD, 20892, United States.
Dannika DailySection on Molecular Structure and Functional Genomics, National Institutes of Health, National Eye Institute, Bethesda, MD, 20892, United States.
Lijin DongGenetic Engineering Core, National Institutes of Health, National Eye Institute, Bethesda, MD, 20892, United States.
Katherine PetersonSection on Molecular Structure and Functional Genomics, National Institutes of Health, National Eye Institute, Bethesda, MD, 20892, United States.
Robert FarissBiological Imaging Core, National Institutes of Health, National Eye Institute, Bethesda, MD, 20892, United States.
Graeme WistowSection on Molecular Structure and Functional Genomics, National Institutes of Health, National Eye Institute, Bethesda, MD, 20892, United States. Electronic address: wistowg@nih.gov.

Funding

Functional Analysis of Novel Genes in Eye Development and VisionZ01EY000433 · NEI · NATIONAL EYE INSTITUTE · PI WISTOW, GRAEME J · 2005 to 2008
$1.7M
Intramural NIH HHS Z01 EY000433
6 · The paper itself

Abstract

Amelotin (AMTN), a protein involved in enamel formation, is induced in retinal pigment epithelial (RPE) in patients with dry age-related macular degeneration (AMD) and is associated with calcification in drusen. To examine the effects of constitutive expression of human AMTN in RPE we created a transgenic (TG) mouse model that expresses human AMTN specifically in the RPE using the regulatory components of the mouse Rpe65 gene. This led to several AMD-like abnormalities in RPE but did not produce calcified depositions. Reasoning that other aspects of cell stress or damage may be needed for calcification we tested moderate laser injury of the retina in young TG and WT mice. TG mice, but not WT, developed AMTN-dependent deposits containing AMTN, cholesterol, and calcium phosphate/HAP in the laser lesions, reminiscent of deposits seen in dry AMD drusen. While laser lesions in WT mice healed normally, those in TG mice progressed, obliterating adjacent photoreceptors and recruiting microglia. This shows that chronic expression of AMTN can induce pathologies in RPE and that when coupled with injury can form structures similar to calcified drusen. These deposits are associated with increased retinal damage and inflammation. The model presents a system to test possible therapeutic effects of inhibition or suppression of AMTN in RPE in vivo.

Indexed as

CalcinosisDisease Models, AnimalGeographic AtrophyMacular DegenerationRetinal Pigment EpitheliumAnimalsCalcium PhosphatesCholesterolHumansMiceMice, Inbred C57BLMice, TransgenicCalcium PhosphatesCholesterolAge-related macular degenerationAmelotinCalcium phosphateDisease modelsDrusenHydroxyapatiteMouse models

Identifiers

PMID42134448
PMCPMC13209737

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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.