GLP-1 Receptor Agonist NLY01 Reduces Retinal Inflammation and Neuron Death Secondary to Ocular Hypertension
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Abstract
Glaucoma is the leading cause of irreversible blindness and is characterized by the death of retinal ganglion cells (RGCs). Recent studies have implicated pro-inflammatory microglia, macrophages, and A1 astrocytes in the pathogenesis of neurodegenerative diseases. The role of pro-inflammatory, neurotoxic A1 astrocytes in glaucoma is just beginning to be explored. Using a mouse model of glaucoma, we demonstrate that ocular hypertension is sufficient to trigger production of C1q, interleukin-1α (IL-1α), and tumor necrosis factor α (TNF-α), three cytokines necessary and sufficient to drive the formation of A1 astrocytes. Upregulation of these cytokines occurs first in CD11b + CD11c + cells followed by CD11b + CD11c − cells. Ablation of this pathway, by either genetic deletions of C1qa, IL-1α, and TNF-α, or treatment with glucagon-like peptide-1 receptor agonist NLY01, reduces A1 astrocyte transformation and RGC death. Together, these results highlight a neuroinflammatory mechanism of glaucomatous neurodegeneration that can be therapeutically targeted by NLY01 administration.
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Elovl1 cKO mice still showed neuronal death following ONC, unlike Il1a−/−Tnf−/−C1qa−/− mice, which show no RGC death following axon crush, but the amount of death was reduced.
“While Elovl1 cKO mice still showed neuronal death following ONC (unlike in Il1a−/−Tnf−/−C1qa−/− mice, which show no RGC death following axon crush2,3,20), the amount of death was reduced”
From Neurotoxic reactive astrocytes induce cell death via saturated lipids (2021) · cites this paper as [20]
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- Authors
- Sterling, J. K., Adetunji, M. O., Guttha, S., Bargoud, A. R., Uyhazi, K. E., Ross, A. G., Dunaief, J. L., & Cui, Q. N.
- Affiliations
- University of Pennsylvania (US)
- University of Pennsylvania Health System (US)
- Corresponding author
- Sterling, Jacob K.
- Cui, Qi N.
- ORCID
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2020-11
- Volume
- 33
- Issue
- 5
- Pages
- 108271
- ISSN
- 2211-1247 (ISSN-L)
- PMC
- PMC7660987
- OpenAlex
- W3096251629
- Cited by
- 148
- References
- 52
- Citations by year
- 2026: 30 · 2025: 31 · 2024: 21 · 2023: 24 · 2022: 20 · 2021: 22
- FWCI
- 13.10
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cell Reports (publishedVersion, cc-by)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institutes of Health (R01EY015240, R01EY028916)
- Research to Prevent Blindness
- American Glaucoma Society (T32EY007035, T32GM007170)
- Paul MacKall and Evanina Bell MacKall Trust
- Topics
- Health Sciences › Medicine › Ophthalmology › Glaucoma and retinal disorders
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
- Keywords
- glaucoma, GLP-1 receptor agonists, ocular hypertension, retinal ganglion cell death, neuroinflammation, C1q, interleukin-1 alpha, TNF-α, microglia, macrophages, glaucomatous neurodegeneration
- MeSH terms
- Glucagon-Like Peptide-1 Receptor, Glucagon-Like Peptide-1 Receptor Agonists, Animals, Astrocytes, Female, Inflammation, Intraocular Pressure, Male, Mice, Inbred C57BL, Ocular Hypertension, Retinal Ganglion Cells, Tumor Necrosis Factor-alpha, Complement C1q, Cell Death, CD11b Antigen, Interleukin-1alpha, Retinal Neurons
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