Caveolin-1 defines astrocyte mechanobiology in the glial lamina of the optic nerve head.
4 affiliations
- 1Institute of Human Anatomy and Embryology, University of Regensburg, Regensburg, Germany.
- 2Institute of Neuroanatomy, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
- 3Department of Biochemistry & Physiology, The University of Oklahoma Health Campus, Oklahoma, OK, United States.
- 4Dean A. McGee Department of Ophthalmology, The University of Oklahoma Health Campus, Oklahoma, OK, United States.
Abstract
The optic nerve head is the principal site of retinal ganglion cell axonal injury in primary open angle glaucoma, where astrocyte mechanobiology and extracellular matrix remodeling are thought to play critical roles in disease progression. Caveolae, which are mechanosensitive plasma membrane invaginations formed by Caveolin and Cavin proteins, are key regulators of cellular responses to mechanical stress, yet their involvement in optic nerve head pathophysiology has not been defined. Here, we characterize the presence, regulation, and mechanobiological relevance of Caveolin and Cavin proteins in murine optic nerve astrocytes in vitro and in vivo. Primary optic nerve astrocytes exhibited classical caveolar structures and expressed Caveolin-1, Caveolin-2 and multiple Cavins. In vivo, Caveolin-1 is highly enriched in astrocytes of the glial lamina. Glaucoma-associated factors CCN2/CTGF and TGF-β2 significantly increased Caveolin-1 and Cavin-1 expression in optic nerve astrocytes, while CCN2/CTGF knockdown reduced Caveolin-1 expression. Increasing substratum stiffness enhanced Caveolin-1 expression and altered the subcellular localization of Caveolin-1. Furthermore, Caveolin-1 mRNA expression was increased in the optic nerve head of a glaucoma mouse model, while its protein levels were elevated in the entire optic nerve of the transgenic mice. Together, these findings identify caveolae and Caveolin-1 as mechanosensitive components of optic nerve astrocytes and suggest their involvement in biomechanical and molecular alterations of the glaucomatous optic nerve head. This work provides the first evidence linking astrocyte mechanobiology in the glial lamina to Caveolin-1, highlighting a potential novel contributor to glaucoma pathogenesis.
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BibTeX
@article{hoffmann2026caveolin1,
title = {{Caveolin-1 defines astrocyte mechanobiology in the glial lamina of the optic nerve head.}},
author = {Anja K Hoffmann and Anna Dlugosch and Michelle C Geigenfeind and Amelie Seemann and Michael H Elliott and Rudolf Fuchshofer and Andrea E Dillinger},
journal = {Frontiers in cellular neuroscience},
year = {2026},
month = oct,
doi = {10.3389/fncel.2026.1909639},
url = {https://europepmc.org/article/MED/42908589},
note = {CC BY},
}
RIS
TY - JOUR
TI - Caveolin-1 defines astrocyte mechanobiology in the glial lamina of the optic nerve head.
AU - Anja K Hoffmann
AU - Anna Dlugosch
AU - Michelle C Geigenfeind
AU - Amelie Seemann
AU - Michael H Elliott
AU - Rudolf Fuchshofer
AU - Andrea E Dillinger
PY - 2026
DA - 2026/10/07
JO - Frontiers in cellular neuroscience
DO - 10.3389/fncel.2026.1909639
UR - https://europepmc.org/article/MED/42908589
AB - The optic nerve head is the principal site of retinal ganglion cell axonal injury in primary open angle glaucoma, where astrocyte mechanobiology and extracellular matrix remodeling are thought to play critical roles in disease progression. Caveolae, which are mechanosensitive plasma membrane invaginations formed by Caveolin and Cavin proteins, are key regulators of cellular responses to mechanical stress, yet their involvement in optic nerve head pathophysiology has not been defined. Here, we characterize the presence, regulation, and mechanobiological relevance of Caveolin and Cavin proteins in murine optic nerve astrocytes in vitro and in vivo. Primary optic nerve astrocytes exhibited classical caveolar structures and expressed Caveolin-1, Caveolin-2 and multiple Cavins. In vivo, Caveolin-1 is highly enriched in astrocytes of the glial lamina. Glaucoma-associated factors CCN2/CTGF and TGF-β2 significantly increased Caveolin-1 and Cavin-1 expression in optic nerve astrocytes, while CCN2/CTGF knockdown reduced Caveolin-1 expression. Increasing substratum stiffness enhanced Caveolin-1 expression and altered the subcellular localization of Caveolin-1. Furthermore, Caveolin-1 mRNA expression was increased in the optic nerve head of a glaucoma mouse model, while its protein levels were elevated in the entire optic nerve of the transgenic mice. Together, these findings identify caveolae and Caveolin-1 as mechanosensitive components of optic nerve astrocytes and suggest their involvement in biomechanical and molecular alterations of the glaucomatous optic nerve head. This work provides the first evidence linking astrocyte mechanobiology in the glial lamina to Caveolin-1, highlighting a potential novel contributor to glaucoma pathogenesis.
SN - 1662-5102
ER -