Neuroprotective effects of minocycline against in vitro and in vivo retinal ganglion cell damage

2005 ◽  
Vol 1053 (1-2) ◽  
pp. 185-194 ◽  
Author(s):  
Masamitsu Shimazawa ◽  
Tetsumori Yamashima ◽  
Neeraj Agarwal ◽  
Hideaki Hara
Keyword(s):  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Cell Damage ◽  
Retinal Ganglion ◽  
Neuroprotective Effects

scholarly journals Exosome-Mediated Delivery of the Neuroprotective Peptide PACAP38 Promotes Retinal Ganglion Cell Survival and Axon Regeneration in Rats With Traumatic Optic Neuropathy

2021 ◽  
Vol 9 ◽  
Author(s):  
Tian Wang ◽  
Yiming Li ◽  
Miao Guo ◽  
Xue Dong ◽  
Mengyu Liao ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Optic Neuropathy ◽  
Axon Regeneration ◽  
Retinal Ganglion ◽  
Traumatic Optic Neuropathy ◽  
Fiber Layer

Traumatic optic neuropathy (TON) refers to optic nerve damage caused by trauma, leading to partial or complete loss of vision. The primary treatment options, such as hormonal therapy and surgery, have limited efficacy. Pituitary adenylate cyclase-activating polypeptide 38 (PACAP38), a functional endogenous neuroprotective peptide, has emerged as a promising therapeutic agent. In this study, we used rat retinal ganglion cell (RGC) exosomes as nanosized vesicles for the delivery of PACAP38 loaded via the exosomal anchor peptide CP05 (EXOPACAP38). EXOPACAP38 showed greater uptake efficiency in vitro and in vivo than PACAP38. The results showed that EXOPACAP38 significantly enhanced the RGC survival rate and retinal nerve fiber layer thickness in a rat TON model. Moreover, EXOPACAP38 significantly promoted axon regeneration and optic nerve function after injury. These findings indicate that EXOPACAP38 can be used as a treatment option and may have therapeutic implications for patients with TON.

scholarly journals Mitochondrial pathogenic mechanism and degradation in optineurin E50K mutation-mediated retinal ganglion cell degeneration

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Myoung Sup Shim ◽  
Yuji Takihara ◽  
Keun-Young Kim ◽  
Takeshi Iwata ◽  
Beatrice Y. J. T. Yue ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Open Angle Glaucoma ◽  
Mitochondrial Fission ◽  
Retinal Ganglion ◽  
Cell Degeneration ◽  
Transport Dynamics

Abstract Mutations in optineurin (OPTN) are linked to the pathology of primary open angle glaucoma (POAG) and amyotrophic lateral sclerosis. Emerging evidence indicates that OPTN mutation is involved in accumulation of damaged mitochondria and defective mitophagy. Nevertheless, the role played by an OPTN E50K mutation in the pathogenic mitochondrial mechanism that underlies retinal ganglion cell (RGC) degeneration in POAG remains unknown. We show here that E50K expression induces mitochondrial fission-mediated mitochondrial degradation and mitophagy in the axons of the glial lamina of aged E50K−tg mice in vivo. While E50K activates the Bax pathway and oxidative stress, and triggers dynamics alteration-mediated mitochondrial degradation and mitophagy in RGC somas in vitro, it does not affect transport dynamics and fission of mitochondria in RGC axons in vitro. These results strongly suggest that E50K is associated with mitochondrial dysfunction in RGC degeneration in synergy with environmental factors such as aging and/or oxidative stress.

Neuroprotective Effects of Brimonidine against Transient Ischemia-induced Retinal Ganglion Cell Death: a Dose Response in Vivo Study

2002 ◽  
Vol 74 (2) ◽  
pp. 181-189 ◽  
Author(s):  
M.P. Lafuente ◽  
M.P. Villegas-Pérez ◽  
S. Mayor ◽  
M.E. Aguilera ◽  
J. Miralles de Imperial ◽  
...  
Keyword(s):  
Cell Death ◽  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Dose Response ◽  
Retinal Ganglion ◽  
Transient Ischemia ◽  
Neuroprotective Effects ◽  
Retinal Ganglion Cell Death ◽  
Ganglion Cell Death

Experimental detection of retinal ganglion cell damage in vivo

2009 ◽  
Vol 88 (4) ◽  
pp. 831-836 ◽  
Author(s):  
Christopher Kai-Shun Leung ◽  
Robert N. Weinreb
Keyword(s):  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Cell Damage ◽  
Retinal Ganglion ◽  
Experimental Detection

The role of calpain in an in vivo model of oxidative stress-induced retinal ganglion cell damage

2014 ◽  
Vol 451 (4) ◽  
pp. 510-515 ◽  
Author(s):  
Yu Yokoyama ◽  
Kazuichi Maruyama ◽  
Kotaro Yamamoto ◽  
Kazuko Omodaka ◽  
Masayuki Yasuda ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Cell Damage ◽  
In Vivo Model ◽  
Retinal Ganglion

scholarly journals Optimized OPA1 Isoforms 1 and 7 Provide Therapeutic Benefit in Models of Mitochondrial Dysfunction

2020 ◽  
Vol 14 ◽  
Author(s):  
Daniel M. Maloney ◽  
Naomi Chadderton ◽  
Sophia Millington-Ward ◽  
Arpad Palfi ◽  
Ciara Shortall ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Optic Atrophy ◽  
Therapeutic Interventions ◽  
Fibroblast Cells ◽  
Retinal Ganglion ◽  
Cell Degeneration

Optic Atrophy 1 (OPA1) is a mitochondrially targeted GTPase that plays a pivotal role in mitochondrial health, with mutations causing severe mitochondrial dysfunction and typically associated with Dominant Optic Atrophy (DOA), a progressive blinding disease involving retinal ganglion cell loss and optic nerve damage. In the current study, we investigate the use of codon-optimized versions of OPA1 isoform 1 and 7 as potential therapeutic interventions in a range of in vitro and in vivo models of mitochondrial dysfunction. We demonstrate that both isoforms perform equally well in ameliorating mitochondrial dysfunction in OPA1 knockout mouse embryonic fibroblast cells but that OPA1 expression levels require tight regulation for optimal benefit. Of note, we demonstrate for the first time that both OPA1 isoform 1 and 7 can be used independently to protect spatial visual function in a murine model of retinal ganglion cell degeneration caused by mitochondrial dysfunction, as well as providing benefit to mitochondrial bioenergetics in DOA patient derived fibroblast cells. These results highlight the potential value of OPA1-based gene therapy interventions.

Sign in / Sign up

Export Citation Format

Share Document