Sensory systemMüller glial cells express nestin coupled with glial fibrillary acidic protein in experimentally induced glaucoma in the rat retina
Section snippets
Experimental procedures
A total of 41 adult female Wistar rats (weighing 180∼240g; aged 8 weeks) were used in this study. Food and water were provided ad libitum, and the animals were maintained on a 12-h light/dark cycle. Two rats were used for normal study, 39 rats for experimental glaucoma induction. In the handling and care of all animals, the International Guiding Principles for animals research, as stipulated by the Council for International Organizations of Medical Science (CIOMS) (1985) and as adopted by the
IOP
In the normal and sham-operated control eyes, the baseline IOP of rats was 17.57±0.42 mm Hg. At 2 h after operation, the mean IOP of the experimental eyes was immediately increased to 26.77±1.68 mm Hg. This was further raised with time, peaking at 1 day to reach 27.10±1.27 mm Hg, that was 1.55-fold over baseline. The significant elevation in IOP was sustained throughout the experimental period (P<0.01) (Fig. 1). The ocular tissues including the cornea, lens and sclera appeared structurally
Discussion
Damage of the inner retinal layers leading to the loss of ganglion cells and their axons in glaucomatous models has been well documented using different conventional histological methods as well as apoptotic markers (Glovinsky et al 1993, Garcia-Valenzuela et al 1995, Wygnanski et al 1995, Laquis et al 1998, Wang et al 2000). The present results corroborate this showing a significant loss of NeuN labeled ganglion cells beginning at 1 week postoperation with the rise of the IOP. Concomitant to
Conclusion
In conclusion, the central goal of this study was to examine the reactive changes of Müller glial cells to glaucoma. It is unequivocal that elevated IOP induces Müller glial cell activation as manifested by an increase in GFAP and nestin expression. The induced expression of nestin along with the increased expression of GFAP in Müller glial cells may reflect a metabolic change of the cells in response to the degenerative changes of their neighboring ganglion cells whose functions are closely
References (34)
- et al.
Identification of neural progenitors in the adult mammalian eye
Biochem Biophys Res Commun
(2000) - et al.
MK801a neuroprotectant in rat hypertensive eyes
Brain Res
(1998) - et al.
Programmed cell death of retinal ganglion cells during experimental glaucoma
Exp Eye Res
(1995) - et al.
Expression of glial fibrillary acidic protein (GFAP), glutamine synthetase (GS), and Bcl-2 protooncogene protein by Müller (glial) cells in retinal light damage of rats
Neurosci Lett
(1995) Riding the glial monoraila common mechanism for glial-guided neuronal migration in different regions of the developing mammalian brain
Trends Neurosci
(1990)- et al.
Making heads and tails of intermediate filament assembly, dynamics and networks
Curr Opin Cell Biol
(1994) - et al.
The patterns of retinal ganglion cell death in hypertensive eyes
Brain Res
(1998) Glaucomachanging concepts and future directions
Mayo Clin Proc
(1996)- et al.
NMDA receptors in cultured radial glia
FEBS Lett
(1997) - et al.
The Müller cella functional element of the retina
Trends Neurosci
(1996)
Distribution of glutamate receptor subtypes in the vertebrate retina
Neuroscience
What do retinal Müller (glial) cells do for their neuronal ‘small siblings’?
J Chem Neuroanat
Comparison of ganglion cell loss and cone loss in experimental glaucoma
Am J Ophthalmol
Macrophages, microglia, and astrocytes are rapidly activated after crush injury of the goldfish optic nervea light and electron microscopic analysis
J Comp Neurol
Müller cell expression of glial fibrillary acidic protein after genetic and experimental photoreceptor degeneration in the rat retina
Invest Ophthalmol Vis Sci
Transitin, a nestin-related intermediate filament, is expressed by neural progenitors and can be induced in Müller glia in the chicken retina
J Comp Neurol
Rapid, widespread, and longlasting induction of nestin contributes to the generation of glial scar tissue after CNS injury
J Cell Biol
Cited by (91)
Activation of retinal glial cells contributes to the degeneration of ganglion cells in experimental glaucoma
2023, Progress in Retinal and Eye ResearchProgressive degeneration of the retina in Loxl3 mutant mouse model of Stickler syndrome
2023, Developmental BiologyNeuroprotective effects of DAAO are mediated via the ERK1/2 signaling pathway in a glaucomatous animal model
2020, Experimental Eye ResearchCitation Excerpt :All those increased expressions of cytokines are cytotoxic for RGCs (Bringmann et al., 2006). GFAP-positive cells are mainly astrocytes, and in pathological conditions, such as in the COH model, Müller cells vigorously express GFAP, which they do not express in normal conditions (Xue et al., 2006; Ji et al., 2012). Neuroprotective therapies were used to reduce RGC apoptosis in response to increased IOP in the ischemia/reperfusion rat model, accompanied by reduced GFAP expression (Fernandez et al., 2009; Igarashi et al., 2016; Li et al., 2018).
Müller cells as a target for retinal therapy
2019, Drug Discovery Today