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Updated: Aug 12, 2026
Retinal Detachment Model in Rodents by Subretinal Injection of Sodium Hyaluronate
Published on: September 11, 2013
Preventing retinal detachment-associated photoreceptor cell loss in Bax-deficient mice
Liu Yang1, Deisy Bula, Jorge G Arroyo
1Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts 02114, USA.
Purpose:
To characterize photoreceptor cell apoptosis and cell loss in a mouse model of experimental retinal detachment (RD), and to use the technology of mouse genetics to study the molecular mechanisms underlying RD-associated photoreceptor degeneration.
Methods:
Retinal detachments were created in adult wild-type and Bax-deficient mice by subretinal injection of 1.4% sodium hyaluronate. At 1, 3, 7, and 28 days after injection, animals were killed, eyes enucleated, and retinal sections studied by histochemistry, immunofluorescence labeling, and confocal microscopy. Rods and cones were labeled, and apoptotic cells were identified with terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL). Photoreceptor cell apoptosis and cell loss were assessed quantitatively by counting both surviving and TUNEL-positive rods and cones.
Results:
TUNEL-positive cells were found within the outer nuclear layer (ONL) of the detached portions of the retina. They were detected in the detached retina on day 1, peaked on day 3, and dropped precipitously after day 7 after RD. Photoreceptor cell loss of both rods and cones followed a similar time course after RD. Moreover, deletion of the proapoptotic gene Bax in a knockout mouse model abolished the RD-associated photoreceptor cell degeneration.
Conclusions:
Apoptosis is a major mechanism leading to photoreceptor cell death after RD. Blockage of the activity of the proapoptotic molecule Bax in a knockout mouse model prevents photoreceptor cell apoptosis and cell loss. These data suggest that the Bax-mediated apoptotic signaling pathway plays a critical role in RD-associated photoreceptor cell death.
Insights
Experimental retinal detachment causes photoreceptor cell death through apoptosis. Blocking the Bax gene prevents this cell loss, highlighting Bax
Area of Science:
- Ophthalmology
- Molecular Biology
- Genetics
Background:
- Retinal detachment (RD) can lead to photoreceptor degeneration.
- Understanding the molecular mechanisms of photoreceptor cell death in RD is crucial for developing treatments.
Purpose of the Study:
- To investigate photoreceptor cell apoptosis and loss in a mouse model of experimental retinal detachment.
- To elucidate the role of the Bax gene in RD-associated photoreceptor degeneration using mouse genetics.
Main Methods:
- Experimental retinal detachment was induced in wild-type and Bax-deficient mice.
- Histochemistry, immunofluorescence, and TUNEL staining were used to identify and quantify apoptotic photoreceptor cells.
- Photoreceptor cell loss was assessed quantitatively at multiple time points post-RD.
Main Results:
- Apoptotic cells were detected in the outer nuclear layer of detached retinas, peaking at day 3 and decreasing after day 7.
- Both rod and cone photoreceptor cell loss followed a similar time course.
- Bax-deficient mice showed no significant photoreceptor cell degeneration after RD.
Conclusions:
- Apoptosis is a primary mechanism of photoreceptor cell death following retinal detachment.
- The proapoptotic molecule Bax plays a critical role in RD-associated photoreceptor degeneration.
- Inhibition of Bax-mediated apoptosis prevents photoreceptor cell death in experimental RD.
