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Updated: Feb 3, 2026
Isolation of Primary Mouse Retinal Glial Müller Cells
Published on: August 30, 2024
CRISPR-mediated SOX9 knockout inhibits GFAP expression in retinal glial (Müller) cells
Xin Wang1, Qinmeng Shu1, Yingqin Ni1
1Department of Ophthalmology and Vision Sciences, Eye and ENT Hospital, Shanghai Medical College.
Abstract:
Müller cells, as the predominant glial element in the sensory retina, play a crucial role in healthy and diseased retina. Overactivation of Müller cells in response to damage is detrimental to the retina tissue. Current research shows that inhibiting glial fibrillary acidic protein (GFAP), a sensitive indicator of Müller cell activation, attenuated glial reactions and promoted neuroprotection. Recent evidence suggests that the transcript factor SOX9 (sex-determining region Y box 9), part of the SOX family, regulates GFAP expression of astrocytes in the central nervous system. However, in retina Müller cells, it is still unknown whether GFAP can be downregulated by reduced SOX9 function. The present results show that clustered regularly interspaced short palindromic repeats/Cas9-mediated SOX9 knockout not only inhibited GFAP expression in rat Müller cells but also attenuated cell migration ability. These results suggest that inhibition of SOX9 activity may be a novel therapeutic strategy for reduction of glial cell activity.
Insights
Inhibiting SOX9 function reduces glial fibrillary acidic protein (GFAP) expression and cell migration in rat Müller cells. This suggests targeting SOX9 may offer a new therapeutic approach for retinal diseases.
Area of Science:
- Neuroscience
- Ophthalmology
- Cell Biology
Background:
- Müller cells are key glial cells in the retina, crucial for its function and disease response.
- Overactivated Müller cells contribute to retinal damage, and inhibiting glial fibrillary acidic protein (GFAP) shows neuroprotective effects.
- SOX9 (sex-determining region Y box 9) regulates GFAP in astrocytes, but its role in Müller cells is unclear.
Purpose of the Study:
- To investigate whether SOX9 inhibition can downregulate GFAP expression in retinal Müller cells.
- To determine the effect of SOX9 function on Müller cell activation and migration.
Main Methods:
- Utilized clustered regularly interspaced short palindromic repeats/Cas9 (CRISPR/Cas9) technology for SOX9 knockout in rat Müller cells.
- Assessed GFAP expression levels and cell migration ability post-SOX9 knockout.
Main Results:
- CRISPR/Cas9-mediated SOX9 knockout significantly inhibited GFAP expression in rat Müller cells.
- Reduced SOX9 function also attenuated the migratory capacity of Müller cells.
- These findings link SOX9 activity to GFAP regulation and Müller cell behavior.
Conclusions:
- SOX9 plays a role in regulating GFAP expression and cell migration in retinal Müller cells.
- Inhibiting SOX9 activity presents a potential novel therapeutic strategy for managing excessive glial cell activity in retinal conditions.
- Further research into SOX9 modulation could lead to new treatments for retinal diseases.
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