OSCR

Galectin-3 is elevated in Müller glia in human glaucomatous eyes and ocular hypertensive rat eyes and associated with phagocytosing states.

Overview

Authors: Anne Rombaut1, Luozixian Wang2,3, Emma Lardner1, Raymond CB Wong2,3, Charlotte Taul4, Miriam Kolko4,5,6, Gustav Stålhammar1, Rune Brautaset1, Filippo Locri1, Pete A. Williams1,2, James R. Tribble1,7
ORCID iDs: Miriam Kolko, James R. Tribble
  1. Department of Clinical Neuroscience, Division of Eye and Vision, St. Erik Eye Hospital, Karolinska Institutet,Stockholm, Sweden
  2. Centre for Eye Research Australia, Royal Victorian Eye and Ear Hospital,Melbourne, Australia
  3. Department of Surgery (Ophthalmology), The University of Melbourne,Melbourne, Australia
  4. Department of Drug Design and Pharmacology, University of Copenhagen,Copenhagen, Denmark
  5. Department of Ophthalmology, Copenhagen University Hospital,Glostrup, Denmark
  6. Department of Ophthalmology, Aalborg University Hospital,Aalborg, Denmark
  7. Wolfson Sensory, Pain and Regeneration Centre (SPaRC), School of Neuroscience, King’s College London,London, UK
Institutions: Karolinska Institutet (Sweden); The Royal Victorian Eye & Ear Hospital (Australia); The University of Melbourne (Australia); University of Copenhagen (Denmark); Copenhagen University Hospital (Denmark); Aalborg University Hospital (Denmark); King's College London (United Kingdom)
Journal: Acta neuropathologica communications, volume 14, issue 1, article 159
Dates: received 19 March 2026; accepted 15 July 2026; published online 4 August 2026
Type: Research article · Language: English
License: CC BY
Identifiers: DOI 10.1186/s40478-026-02388-7 · PMID 42552556 · PMCID PMC13439881 · OpenAlex W7172421825
Open access: gold, a free copy (OpenAlex)
Status: data only
Categories: human (organism), rat (organism), other condition (population), cellular / molecular (subfield)
Methods: Spectral & time-frequency, Statistics, Smoothing, state filtering, decompositions
Keywords: Retina, Glaucoma, Galectin-3, Astrocyte, Microglia, Müller glia, Neuroinflammation, Phagocytosis
MeSH: Ependymoglial Cells*, Galectin 3*, Glaucoma*, Ocular Hypertension*, Phagocytosis*, Aged, Animals, Blood Proteins, Calcium-Binding Proteins, Disease Models, Animal, Female, Galectins, Glial Fibrillary Acidic Protein, Humans, Male, Microfilament Proteins, Microglia, Middle Aged, Rats, Rats, Sprague-Dawley (* major topic)
Topic: Galectins and Cancer Biology (Immunology, Immunology and Microbiology), according to OpenAlex
Funding: Karolinska Institute
Citations: not cited yet (Europe PMC); 51 references in the paper

Abstract

Glaucoma is a leading cause of irreversible blindness worldwide, yet available treatments fail to prevent disease progression for all patients. It is characterized by a progressive dysfunction and loss of retinal ganglion cells. Neuroinflammation has been recognized as an underlying neurodegenerative mechanism of glaucoma in animal models and human post-mortem samples, and targeting neuroinflammation may provide additional means to neuroprotection. Galectin-3, a pro-inflammatory mediator encoded by the LGALS3 gene in humans, holds promise as a treatable target as its pharmacological and genetic inhibition is neuroprotective in multiple models of experimental glaucoma. However, the role of Galectin-3 in glaucoma remains unclear, particularly whether its emergence is a consequence of degeneration, or occurs at earlier time points. To address these knowledge gaps, we labeled IBA1, GFAP, and Galectin-3 in retina sections at early glaucoma stages in the rat bead glaucoma model, and in human retina from glaucoma donors. In the rat, IBA1 volume, but not GFAP, increased at an early, pre-degenerative timepoint. Accompanying this, we identified a significant increase of Galectin-3/IBA1 colocalization compared to control at the same timepoint, supporting the upregulation of Galectin-3 in early inflammation, preceding retinal ganglion cell degeneration in experimental glaucoma. However, a significant increase in Galectin-3/GFAP colocalization compared to control at the same timepoint in the rat additionally associates Galectin-3 production with astrocytes and Müller glia. This Galectin-3 to Müller glia relationship was significantly pronounced in human glaucomatous retina, predominating over microglia co-labelling. We further demonstarted that human MIO-M1 Müller glia in vitro express Galectin-3, but this is not altered in response to glaucoma relevant stimuli (TNF-α or mild-metabolic stress from rotenone). Instead, Galectin-3 expression was altered in phagocytosing states from exposure to E. coli particles, brain synaptosomes, or apoptotic neuronal debris. These findings provide further insight into Galectin-3 and gross inflammatory responses in glaucoma pathology.

Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1186/s40478-026-02388-7.

Reproduced under the paper's license (CC BY), from the paper cited above.

Code

The paper links to its data, not to its authors' code: see the Data section.

Tracing map

A tracing map links a paper to the code its authors published: this paper has none, so it has no map.

Data

Datasets cited

Data availability

All data generated during this study are included in this published article and its supplementary information files. The nuRNAseq dataset from Orozco *et al.*, analyzed in the current study is available in the Gene Expression Omnibus (GEO) repository, through NCBI GEO ([https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE135133]). Reference number: GSE135133. The nuRNAseq dataset from Li *et al.*, analyzed in the current study is available in the Human Cell Atlas Data Portal repository (Human Retina Cell Atlas v1.0: available at https://data.humancellatlas.org/hca-bio-networks/eye/atlases/retina-v1-0).

Reproduced under the paper's license (CC BY), from the paper cited above.

Versions

The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.

Version 1, 27 September 2026: the first record

Recorded: type, language, journal, volume, issue, pages, dates, 11 authors, 8 keywords, 20 MeSH terms, 1 funder, 49 references.

Cite

This paper

Rombaut, A., Wang, L., Lardner, E., Wong, R. C., Taul, C., Kolko, M., Stålhammar, G., Brautaset, R., Locri, F., Williams, P. A., & Tribble, J. R. (2026). Galectin-3 is elevated in Müller glia in human glaucomatous eyes and ocular hypertensive rat eyes and associated with phagocytosing states. Acta neuropathologica communications, 14(1), 159. https://doi.org/10.1186/s40478-026-02388-7

BibTeX

@article{rombaut2026galectin,
author = {Rombaut, Anne and Wang, Luozixian and Lardner, Emma and Wong, Raymond CB and Taul, Charlotte and Kolko, Miriam and Stålhammar, Gustav and Brautaset, Rune and Locri, Filippo and Williams, Pete A. and Tribble, James R.},
title = {{Galectin-3 is elevated in Müller glia in human glaucomatous eyes and ocular hypertensive rat eyes and associated with phagocytosing states}},
journal = {Acta neuropathologica communications},
year = {2026},
month = aug,
volume = {14},
number = {1},
pages = {159},
publisher = {BMC},
issn = {2051-5960},
doi = {10.1186/s40478-026-02388-7},
url = {https://doi.org/10.1186/s40478-026-02388-7},
pmid = {42552556},
pmcid = {PMC13439881}
}

RIS

TY - JOUR
AU - Rombaut, Anne
AU - Wang, Luozixian
AU - Lardner, Emma
AU - Wong, Raymond CB
AU - Taul, Charlotte
AU - Kolko, Miriam
AU - Stålhammar, Gustav
AU - Brautaset, Rune
AU - Locri, Filippo
AU - Williams, Pete A.
AU - Tribble, James R.
TI - Galectin-3 is elevated in Müller glia in human glaucomatous eyes and ocular hypertensive rat eyes and associated with phagocytosing states
T2 - Acta neuropathologica communications
J2 - Acta Neuropathol Commun
PY - 2026
DA - 2026/08/04
VL - 14
IS - 1
SP - 159
SN - 2051-5960
PB - BMC
DO - 10.1186/s40478-026-02388-7
UR - https://doi.org/10.1186/s40478-026-02388-7
LA - en
ER -

CSL-JSON

{
"id": "10.1186/s40478-026-02388-7",
"type": "article-journal",
"title": "Galectin-3 is elevated in Müller glia in human glaucomatous eyes and ocular hypertensive rat eyes and associated with phagocytosing states",
"container-title": "Acta neuropathologica communications",
"author": [
{
"family": "Rombaut",
"given": "Anne"
},
{
"family": "Wang",
"given": "Luozixian"
},
{
"family": "Lardner",
"given": "Emma"
},
{
"family": "Wong",
"given": "Raymond CB"
},
{
"family": "Taul",
"given": "Charlotte"
},
{
"family": "Kolko",
"given": "Miriam"
},
{
"family": "Stålhammar",
"given": "Gustav"
},
{
"family": "Brautaset",
"given": "Rune"
},
{
"family": "Locri",
"given": "Filippo"
},
{
"family": "Williams",
"given": "Pete A."
},
{
"family": "Tribble",
"given": "James R."
}
],
"container-title-short": "Acta Neuropathol Commun",
"volume": "14",
"issue": "1",
"page": "159",
"DOI": "10.1186/s40478-026-02388-7",
"PMID": "42552556",
"PMCID": "PMC13439881",
"ISSN": "2051-5960",
"publisher": "BMC",
"URL": "https://doi.org/10.1186/s40478-026-02388-7",
"language": "en",
"issued": {
"date-parts": [
[
2026,
8,
4
]
]
}
}

Similar papers

The papers with a page that share the most with this one: the tools found in their code, their categories, datasets, cited references and authors, the rarest counting most.

[1] doi:10.1021/acsmedchemlett.6c00058
Potent Neuronal Nicotinamide Adenine Dinucleotide-Boosting Tetrahydroquinoxalines: Structure-Activity Relationships and Early Drug Metabolism and Pharmacokinetics Evaluation.
Journal: ACS medicinal chemistry letters
In common: 2 references
[2] doi:10.1111/acel.70419
Silencing of the Metabolic Gene HKDC1 Is Associated With Aging and Neurodegeneration in Mice and Humans.
Journal: Aging cell
In common: other condition, cellular / molecular, 1 reference
[3] doi:10.1371/journal.pone.0349951
Disentangling crossing fibers with advanced dMRI methods reveals bundle-specific degeneration across the visual system in asymmetric glaucoma.
Journal: PloS one
In common: other condition, 1 reference
[4] doi:10.1016/j.isci.2026.115687
Wasteosomes (corpora amylacea) of the human brain accumulate in CD44-positive astrocytes.
Journal: iScience
In common: cellular / molecular, 1 reference
[5] doi:10.1126/sciadv.aeg3223 [code]
The extreme diversity of retinal amacrine cells has deep evolutionary roots.
Journal: Science advances
In common: cellular / molecular, 1 reference
[6] doi:10.1038/s43587-026-01154-7
Spatial mapping and senolytic targeting of senescent and disease-associated microglia in aged mouse brain white matter.
Journal: Nature aging
In common: cellular / molecular, 1 reference
[7] doi:10.1111/jnc.70420
Loss of Kv8.2 in the Mouse Retina Is Associated With Altered One-Carbon Metabolism.
Journal: Journal of neurochemistry
In common: cellular / molecular, 1 reference
[8] doi:10.1167/iovs.67.8.61 [code]
A Shared Genetic Basis Underlying Myopia-Exotropia Comorbidity.
Journal: Investigative ophthalmology & visual science
In common: 1 reference
[9] doi:10.1038/s41467-026-74171-0 [code]
Cluster replicability in single-cell and single-nucleus atlases of the mouse brain.
Journal: Nature communications
In common: cellular / molecular, 1 reference
[10] doi:10.1038/s41467-026-76112-3
Photostimulation improves maturation of human photoreceptors.
Journal: Nature communications
In common: 1 reference

Contribute

The authors of this paper can claim it, correct its record and validate its tracing map, and the maintainers of its code (its owner, or a public member of its organization) correct what it says of their repository; anyone signed in can ask for its removal. Every request goes to OSCR's own machine, which answers it; your account page follows them.

Sign in with ORCID to claim this paper as one of its authors, correct its record or validate its tracing map: when the paper's metadata lists your ORCID iD, you are recognized at once. Maintainers of its code: sign in with GitHub, then claim the repository on your account page.

Request its removal

To ask OSCR to remove this record, the copies of its authors' scripts or its tracing map, use the removal request page: signed in, you say who you are, what to remove and why, then review and confirm the request. Published rules decide every request (how).

Discussion, reproductions, activity

Discussion: questions and error reports about this paper and its code, from signed-in readers and its authors. It opens with sign-in.

Reproductions: reports from readers who ran the authors' code: what they reproduced, with which environment, commit and data. It opens with sign-in.

Activity: what happens around this paper: new versions of its record, its map's validation, discussions and reproductions. It opens with sign-in.