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Updated: May 29, 2025
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Monitoring Astrocyte Reactivity and Proliferation in Vitro Under Ischemic-Like Conditions
Published on: October 21, 2017
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Transient ocular hypertension remodels astrocytes through S100B
Weiran Huang1, Kenji Matsushita1, Rumi Kawashima1
1Department of Ophthalmology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Plos One
|February 5, 2025
Summary
Early glaucoma involves astrocyte weakening, characterized by reduced S100B expression and slender cell morphology. This reversible response precedes significant remodeling, offering insights into optic nerve degeneration.
Area of Science:
- Ophthalmology
- Neuroscience
- Cell Biology
Background:
- Glaucoma involves progressive optic nerve degeneration and poorly understood astrocyte remodeling.
- Mechanical stress from increased intraocular pressure (IOP) is implicated in glaucoma pathogenesis.
Purpose of the Study:
- Investigate astrocyte morphology under mechanical stress.
- Identify early cellular changes preceding astrocyte remodeling in glaucoma.
- Explore the role of S100B in astrocyte response to stress.
Main Methods:
- Established transient ocular hypertension (OHT) mouse model and in vitro cell stretch model.
- Utilized GFAP, S100B, and actin staining for morphology and cytoskeleton analysis.
- Performed qPCR for gene expression and RNA sequencing after S100B silencing.
Main Results:
- Early OHT and in vitro stretching induced astrocyte contraction, fewer processes, and elongated cell bodies.
- Decreased GFAP intensity and S100B mRNA expression were observed in early OHT.
- S100B downregulation and slender morphology were consistent in vivo and in vitro; S100B silencing mimicked these changes.
- RNA-seq revealed altered gene expression related to metabolism, morphogenesis, and histone modification.
Conclusions:
- Astrocyte S100B downregulation is an early response to mechanical stress, leading to a 'weakened' slender morphology.
- S100B plays a role in astrocyte structural changes and transcriptional alterations under stress.
- Stress-induced astrocyte changes are reversible, with potential for late-stage reactivation linked to S100B.
