Up-regulation of crystallins is involved in the neuroprotective effect of wolfberry on survival of retinal ganglion cells in rat ocular hypertension model

2010 ◽  
pp. n/a-n/a ◽  
Author(s):  
Kin Chiu ◽  
Yuan Zhou ◽  
Sze-Chun Yeung ◽  
Carmen Ka-Ming Lok ◽  
Owen O-Cheung Chan ◽  
...  
Keyword(s):  
Ocular Hypertension ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Neuroprotective Effect ◽  
Retinal Ganglion

scholarly journals MicroRNA-93/STAT3 signalling pathway mediates retinal microglial activation and protects retinal ganglion cells in an acute ocular hypertension model

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yayi Wang ◽  
Shida Chen ◽  
Jiawei Wang ◽  
Yaoming Liu ◽  
Yang Chen ◽  
...  
Keyword(s):  
Ocular Hypertension ◽  
Retinal Ganglion Cells ◽  
Microglial Activation ◽  
Ganglion Cells ◽  
Neuroprotective Effect ◽  
Retinal Ganglion ◽  
Neuroprotective Therapy ◽  
Retinal Microglia

AbstractGlaucoma is a common neurodegenerative disease and a leading cause of irreversible blindness worldwide. Retinal microglia-mediated neuroinflammation is involved in the process of optic nerve damage, but the mechanisms driving this microglial activation remain mostly elusive. Previous investigations reported that microRNAs are associated with the retinal microglial reaction and neural apoptosis. In the present study, we found that microRNA-93-5p (miR-93) played a key role in the reaction of retinal microglial cells in vivo and in vitro. The miR-93 level was significantly reduced in the retinae of rat acute ocular hypertension (AOH) models, which were accompanied by retinal microglial activation, overproduction of inflammatory cytokines, and subsequent retinal ganglion cells (RGCs) death, versus the retinae of controls. The induction of miR-93 overexpression significantly reduced microglial proliferation, migration and cytokine release, inhibited the expression of the target gene signal transducer and activator of transcription 3 (STAT3) and p-STAT3, and was associated with a reduced loss of RGCs. Treatment with a STAT3 inhibitor also decreased retinal microglial activation after AOH injury. Taken together, these results suggest that the miR-93/STAT3 pathway is directly related to the downregulation of retinal microglia-mediated neuro-inflammation and showed a neuroprotective effect. Regulating microglial activation through miR-93 may serve as a target for neuroprotective therapy in pathological ocular hypertension.

Neuroprotective effect of 5ɑ-androst-3β,5,6β-triol on retinal ganglion cells in a rat chronic ocular hypertension model

2017 ◽  
Vol 660 ◽  
pp. 90-95 ◽  
Author(s):  
Yan-Qiu Chen ◽  
Shu-Min Zhong ◽  
Shu-Ting Liu ◽  
Feng Gao ◽  
Fang Li ◽  
...  
Keyword(s):  
Ocular Hypertension ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Neuroprotective Effect ◽  
Retinal Ganglion

scholarly journals Neuroprotection of retinal ganglion cells by the sigma-1 receptor agonist pridopidine in models of experimental glaucoma

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Michal Geva ◽  
Noga Gershoni-Emek ◽  
Luana Naia ◽  
Philip Ly ◽  
Sandra Mota ◽  
...  
Keyword(s):  
Ganglion Cell ◽  
Retinal Degeneration ◽  
Retinal Ganglion Cells ◽  
Retinal Ganglion Cell ◽  
Ganglion Cells ◽  
Neuroprotective Effect ◽  
Retinal Ganglion ◽  
Cell Degeneration ◽  
Sigma 1 Receptor ◽  
Sigma 1

AbstractOptic neuropathies such as glaucoma are characterized by retinal ganglion cell (RGC) degeneration and death. The sigma-1 receptor (S1R) is an attractive target for treating optic neuropathies as it is highly expressed in RGCs, and its absence causes retinal degeneration. Activation of the S1R exerts neuroprotective effects in models of retinal degeneration. Pridopidine is a highly selective and potent S1R agonist in clinical development. We show that pridopidine exerts neuroprotection of retinal ganglion cells in two different rat models of glaucoma. Pridopidine strongly binds melanin, which is highly expressed in the retina. This feature of pridopidine has implications to its ocular distribution, bioavailability, and effective dose. Mitochondria dysfunction is a key contributor to retinal ganglion cell degeneration. Pridopidine rescues mitochondrial function via activation of the S1R, providing support for the potential mechanism driving its neuroprotective effect in retinal ganglion cells.

scholarly journals The effect of celastrol on the ocular hypertension-induced degeneration of retinal ganglion cells

2018 ◽  
Vol 670 ◽  
pp. 89-93 ◽  
Author(s):  
Lei Gu ◽  
Jacky M.K. Kwong ◽  
Daniel Yadegari ◽  
Fei Yu ◽  
Joseph Caprioli ◽  
...  
Keyword(s):  
Ocular Hypertension ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Retinal Ganglion
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