Reaction of Müller cells in an experimental rat model of increased intraocular pressure following timolol, latanoprost and brimonidine

Vidal, Lourdes; Díaz, F.; Villena, Alicia; Moreno, Mercedes; Campos, J. García; Vargas, I. Pérez de

doi:10.1016/j.brainresbull.2010.02.011

Cited by 41 publications

(28 citation statements)

References 52 publications

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“…Wheeler et al (2003) have shown that treatment with brimonidine is associated with neuroprotective effects on RGCs loss in different experimental models of glaucoma. Accordingly, work by Villena et al (2009) andVidal et al (2010) supported the retinal neuroprotective effect of brimonidine. In particular, Vidal et al (2010) have shown that hypotensive drugs attenuate retinal gliosis.…”

Section: Neuroprotectantsmentioning

confidence: 89%

“…Accordingly, work by Villena et al (2009) andVidal et al (2010) supported the retinal neuroprotective effect of brimonidine. In particular, Vidal et al (2010) have shown that hypotensive drugs attenuate retinal gliosis. More recently, Jung et al (2015) reported that brimonidine decreases RGC apoptosis upregulating EAAT1 and downregulating NMDA receptors.…”

Section: Neuroprotectantsmentioning

confidence: 89%

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New strategies for neuroprotection in glaucoma, a disease that affects the central nervous system

Nucci

Russo

Martucci

et al. 2016

European Journal of Pharmacology

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a b s t r a c tGlaucoma is a disease where retinal ganglion cells (RGC) are specifically affected though a number of evidences endorse the hypothesis that glaucoma is a neuro-degenerative disorder of the central nervous system and suggest a possible connection between glaucomatous damage and cerebrovascular alterations. The mechanisms underlying RGC loss are not yet fully known but alterations of the autophagy machinery have been recently proposed as a potential contributing factor as for Alzheimer's disease.Here we review the current literature on new strategies for neuroprotection in glaucoma, focusing on pharmacologic strategies to minimize RGC damage.

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Section: Neuroprotectantsmentioning

confidence: 89%

Section: Neuroprotectantsmentioning

confidence: 89%

New strategies for neuroprotection in glaucoma, a disease that affects the central nervous system

Nucci

Russo

Martucci

et al. 2016

European Journal of Pharmacology

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“…During retinal injury, Műller cells are well known to undergo reactive gliosis characterized by the upregulation of GFAP (19). Műller cells, the main type of glial cell in the retina, are responsible for the maintenance of homeostasis in the extracellular medium of the retina, and protect the neurons by releasing neurotrophic factors and secreting glutathione, which has an antioxidant effect (23). The relative delayed reaction of Műller cells, as compared with those of the adult rats, may contribute to the increased vulnerability of immature retina to HI injury.…”

Section: Hypoxic-ischemic Retinal Injurymentioning

confidence: 99%

Hypoxic–ischemic retinal injury in rat pups

Huang

Hung

et al. 2012

Pediatr Res

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Background: Visual loss associated with brain damage, especially hypoxic-ischemic (hI) encephalopathy, is the most common cause of visual impairment in children in developed countries. We hypothesized that hI insults can cause long-term damage in immature eyes. Methods: In postnatal day 7 rat pups, hI was induced by unilateral common carotid artery ligation followed by hypoxia. Retina damage was assessed by electroretinography (eRG) and cell counting. Neuronal injury and astrogliosis were evaluated by terminal deoxynucleotidyl transferase nick-end labeling, cleaved caspase 3, eD1, and glial fibrillary acidic protein immunostaining. results: We observed rapid and persistently extensive injuries in the ganglia cell layer (GcL), inner plexiform layer, and inner nuclear layer (INL) in ipsilateral retinas after hI injury, corresponding to the marked alteration in eRG. hI insult caused prominent microglial and Műller cell activation in ipsilateral inner retinas. Neuronal death in the GcL and INL after hI injury was mainly apoptotic, involving caspase-dependent pathways. conclusion: Our study demonstrated the first evidence of hI retinal damage at both the pathological and functional level using the Vannucci model in neonatal rats. Because retinal damage is often associated with hI injury, it is important to demonstrate that a particular neuroprotective strategy effectively preserves the retina in addition to the brain.

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“…Müller cells are responsible for the maintenance of homeostasis in the extracellular medium of the retina and protection of the neurons through the release of neurotrophins (19)(20)(21)(22). Moreover, Müller cells can also have altered expression and functioning potassium channels, with consequential alteration in ion homeostasis and development of edema in the retina.…”

Section: Discussionmentioning

confidence: 99%

In vitro effect of adenosine on the mRNA expression of Kir 2.1 and Kir 4.1 channels in rat retinal Müller cells at elevated hydrostatic pressure

Chen

Wang

et al. 2012

Experimental and Therapeutic Medicine

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Reaction of Müller cells in an experimental rat model of increased intraocular pressure following timolol, latanoprost and brimonidine

Cited by 41 publications

References 52 publications

New strategies for neuroprotection in glaucoma, a disease that affects the central nervous system

New strategies for neuroprotection in glaucoma, a disease that affects the central nervous system

Hypoxic–ischemic retinal injury in rat pups

In vitro effect of adenosine on the mRNA expression of Kir 2.1 and Kir 4.1 channels in rat retinal Müller cells at elevated hydrostatic pressure

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