» Articles » PMID: 23650091

Reversible Reactivity by Optic Nerve Astrocytes

Overview
Journal Glia
Specialty Neurology
Date 2013 May 8
PMID 23650091
Citations 66
Authors
Affiliations
Soon will be listed here.
Abstract

Reactive astrocytes are typically studied in models that cause irreversible mechanical damage to axons, neuronal cell bodies, and glia. Here, we evaluated the response of astrocytes in the optic nerve head to a subtle injury induced by a brief, mild elevation of the intraocular pressure. Astrocytes demonstrated reactive remodeling that peaked at three days, showing hypertrophy, process retraction, and simplification of their shape. This was not accompanied by any significant changes in the gene expression profile. At no time was there discernible damage to the optic axons, as evidenced by electron microscopy and normal anterograde and retrograde transport. Remarkably, the morphological remodeling was reversible. These findings underscore the plastic nature of reactivity. They show that reactivity can resolve fully if the insult is removed, and suggest that reactivity per se is not necessarily deleterious to axons. This reaction may represent very early events in the sequence that eventually leads to glial scarring.

Citing Articles

Role of Microglia in Glaucomatous Pathology.

Somerville M, Garner M, Girkin C, Gross A Adv Exp Med Biol. 2025; 1468:149-153.

PMID: 39930188 DOI: 10.1007/978-3-031-76550-6_25.


A system for producing controlled elevation of intraocular pressure in awake Brown Norway rats.

Morrison J, Cepurna W, Ing E, Johnson E, Abtin A, Wentzien S Exp Eye Res. 2025; 251:110237.

PMID: 39805385 PMC: 11824874. DOI: 10.1016/j.exer.2025.110237.


Extracellular vesicles as emerging players in glaucoma: Mechanisms, biomarkers, and therapeutic targets.

Namdari M, McDonnell F Vision Res. 2024; 226:108522.

PMID: 39581065 PMC: 11640964. DOI: 10.1016/j.visres.2024.108522.


Mechanisms of retinal ganglion cell injury following acute increases in intraocular pressure.

Garner M, Strickland R, Girkin C, Gross A Front Ophthalmol (Lausanne). 2024; 2:1007103.

PMID: 38983517 PMC: 11182138. DOI: 10.3389/fopht.2022.1007103.


Caspase-8-mediated inflammation but not apoptosis drives death of retinal ganglion cells and loss of visual function in glaucomaa.

Guo Y, Verma B, Shrestha M, Marshak-Rothstein A, Gregory-Ksander M Res Sq. 2024; .

PMID: 38947028 PMC: 11213175. DOI: 10.21203/rs.3.rs-4409426/v1.


References
1.
May C, Lutjen-Drecoll E . Morphology of the murine optic nerve. Invest Ophthalmol Vis Sci. 2002; 43(7):2206-12. View

2.
Tsujimura K, Tanaka J, Ando S, Matsuoka Y, Kusubata M, Sugiura H . Identification of phosphorylation sites on glial fibrillary acidic protein for cdc2 kinase and Ca(2+)-calmodulin-dependent protein kinase II. J Biochem. 1994; 116(2):426-34. DOI: 10.1093/oxfordjournals.jbchem.a124542. View

3.
Argaw A, Gurfein B, Zhang Y, Zameer A, John G . VEGF-mediated disruption of endothelial CLN-5 promotes blood-brain barrier breakdown. Proc Natl Acad Sci U S A. 2009; 106(6):1977-82. PMC: 2644149. DOI: 10.1073/pnas.0808698106. View

4.
Sullivan S, Sullivan R, Miller S, Ireland Z, Bjorkman S, Pow D . Phosphorylation of GFAP is associated with injury in the neonatal pig hypoxic-ischemic brain. Neurochem Res. 2012; 37(11):2364-78. DOI: 10.1007/s11064-012-0774-5. View

5.
Howell G, Macalinao D, Sousa G, Walden M, Soto I, Kneeland S . Molecular clustering identifies complement and endothelin induction as early events in a mouse model of glaucoma. J Clin Invest. 2011; 121(4):1429-44. PMC: 3069778. DOI: 10.1172/JCI44646. View