Evidence map›Paper›PMID 28446179›Full record

ArticleJournal of neuroinflammation2017

GlyCAM1 negatively regulates monocyte entry into the optic nerve head and contributes to radiation-based protection in glaucoma.

Pete A Williams, Catherine E Braine, Nicole E Foxworth, Kelly E Cochran, Simon W M John

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

28 citing papers in PubMed, 37 citations in OpenAlex.

  1. Neuroinflammation in glaucoma: a myriad of cellular pathways and players.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
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  18. Immune responses to injury and their links to eye disease.Translational research : the journal of laboratory and clinical medicine · 2021
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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

5 authors at 2 institutions in 1 country.

Pete A WilliamsThe Jackson Laboratory, Bar Harbor, ME, USA.
Catherine E BraineThe Jackson Laboratory, Bar Harbor, ME, USA.
Nicole E FoxworthThe Jackson Laboratory, Bar Harbor, ME, USA.
Kelly E CochranThe Jackson Laboratory, Bar Harbor, ME, USA.
Simon W M JohnThe Jackson Laboratory, Bar Harbor, ME, USA. simon.john@jax.org.
Jackson Laboratory · USTufts University · US

Funding

Factors Determining Intraocular Pressure and Glaucoma SusceptibilityR01EY011721 · NEI · JACKSON LABORATORY · PI JOHN, SIMON W · 2002 to 2018
$12.4M
FACTORS DETERMINING INTRAOCULAR PRESSURER29EY011721 · NEI · JACKSON LABORATORY · PI JOHN, SIMON W · 1997 to 2001
$227k
NEI NIH HHS R01 EY011721NEI NIH HHS R29 EY011721
6 · The paper itself

Abstract

backgroundWe previously reported a profound long-term neuroprotection subsequent to a single radiation-therapy in the DBA/2J mouse model of glaucoma. This neuroprotection prevents entry of monocyte-like immune cells into the optic nerve head during glaucoma. Gene expression studies in radiation-treated mice implicated Glycam1 in this protection. Glycam1 encodes a proteoglycan ligand for L-selectin and is an excellent candidate to modulate immune cell entry into the eye. Here, we experimentally test the hypothesis that radiation-induced over-expression of Glycam1 is a key component of the neuroprotection.

methodsWe generated a null allele of Glycam1 on a DBA/2J background. Gene and protein expression of Glycam1, monocyte entry into the optic nerve head, retinal ganglion cell death, and axon loss in the optic nerve were assessed.

resultsRadiation therapy potently inhibits monocyte entry into the optic nerve head and prevents retinal ganglion cell death and axon loss. DBA/2J mice carrying a null allele of Glycam1 show increased monocyte entry and increased retinal ganglion cell death and axon loss following radiation therapy, but the majority of optic nerves were still protected by radiation therapy.

conclusionsAlthough GlyCAM1 is an L-selectin ligand, its roles in immunity are not yet fully defined. The current study demonstrates a partial role for GlyCAM1 in radiation-mediated protection. Furthermore, our results clearly show that GlyCAM1 levels modulate immune cell entry from the vasculature into neural tissues. As Glycam1 deficiency has a more profound effect on cell entry than on neurodegeneration, further experiments are needed to precisely define the role of monocyte entry in DBA/2J glaucoma. Nevertheless, GlyCAM1's function as a negative regulator of extravasation may lead to novel therapeutic strategies for an array of common conditions involving inflammation.

Indexed as

AnimalsFemaleGlaucomaMaleMiceMice, Inbred C57BLMice, Inbred DBAMonocytesMucinsOptic DiskOptic NerveMucinssulfated glycoprotein p50GlaucomaGlyCAM1MonocytesRadiation therapyRetinal ganglion cell

Identifiers

PMID28446179
PMCPMC5406973
OpenAlexW2608281831

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.