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Mullerian glia in dystrophic rodent retinas: an immunocytochemical analysis
H J Sheedlo1, D Jaynes, A L Bolan
1Department of Anatomy and Cell Biology, University of North Texas Health Science Center, Fort Worth 76107, USA.
Abstract:
Mullerian glia in retinas of Royal College of Surgeons (RCS) dystrophic rats and retinal degeneration (rd/rd) mice undergo biochemical and morphological alterations concomitant with photoreceptor loss. To follow the fate of Mullerian glia in these degenerating retinas, two Muller cell-specific markers, carbonic anhydrase-C (CAC) and cellular retinaldehyde-binding protein (CRALBP), were examined by light microscopic immunocytochemistry. In retinas of 1- to 12-month-old RCS dystrophic rats, cell bodies in the inner nuclear layer and radial processes were immunostained for CAC, but appeared to diminish with age. In addition, a material in the region of the retinal pigment epithelium (RPE), representing expansion of Muller cell processes into the subretinal space, was immunolabelled for CAC in retinas of 2-month-old and older RCS rats. The CAC-immunoreactive Muller cells seen in retinas of 12-month-old RCS rats were disorganized, as significant photoreceptor degeneration had occurred by this time. In retinas of 6-week-old RCS rats, Muller cells and their processes were immunolabelled for CRALBP, which spanned from the nerve fiber layer (NFL) through the outer nuclear layer. The density of this immunostaining increased, especially in the subretinal space, with advancing age in RCS rats, seen most prominently in retinas of 9-month-old RCS rats and decreased by 12 months. In retinas of rd/rd mice beginning by day 14, minimal CAC- and CRALBP-immunoreactive material was observed in the subretinal space. By 6 weeks, when a majority of the photoreceptors had degenerated, the CAC-staining pattern appeared significantly reduced and patchy. This study showed that Muller cells in degenerating retinas of RCS rats and rd/rd mice ultimately exhibited decreased immunolabelling for CAC and CRALBP at the more advanced stages of retinopathy, which coincided with the loss of photoreceptors. This is in contrast to the progressive increase in glial fibrillary acid protein (GFAP), an intermediate filament protein, throughout the retinal dystrophy in both animal models.
Insights
Muller cells in degenerating rat and mouse retinas show reduced markers carbonic anhydrase-C (CAC) and cellular retinaldehyde-binding protein (CRALBP) as photoreceptors are lost. This contrasts with increased glial fibrillary acid protein (GFAP) during retinal dystrophy.
Area of Science:
- Retinal biology
- Neuroscience
- Cellular and molecular biology
Background:
- Mullerian glia in Royal College of Surgeons (RCS) dystrophic rats and retinal degeneration (rd/rd) mice exhibit biochemical and morphological changes alongside photoreceptor loss.
- Understanding Muller cell fate is crucial for comprehending retinal degeneration mechanisms.
Purpose of the Study:
- To investigate the changes in Mullerian glia during retinal degeneration in RCS rats and rd/rd mice.
- To examine the expression patterns of Muller cell-specific markers, carbonic anhydrase-C (CAC) and cellular retinaldehyde-binding protein (CRALBP), in these models.
Main Methods:
- Light microscopic immunocytochemistry was employed to detect CAC and CRALBP.
- Analysis was performed on retinas from RCS rats and rd/rd mice across various age points.
- Immunolabeling patterns were correlated with the extent of photoreceptor loss and disease progression.
Main Results:
- In RCS rats, CAC and CRALBP immunolabeling in Mullerian glia diminished with age and disease progression.
- Expansion of Muller cell processes into the subretinal space was observed, showing CAC immunolabeling in older RCS rats.
- In rd/rd mice, CAC and CRALBP immunolabeling was minimal in the subretinal space and significantly reduced by 6 weeks.
- A contrasting progressive increase in glial fibrillary acid protein (GFAP) was noted in both models throughout the retinal dystrophy.
Conclusions:
- Mullerian glia in these models exhibit decreased expression of CAC and CRALBP in advanced retinal degeneration stages.
- The observed changes in Muller cell markers coincide with photoreceptor loss, suggesting a role in the degenerative process.
- The differential expression of CAC, CRALBP, and GFAP highlights the complex reactive gliosis response in retinal dystrophy.