PACAP-derived mutant peptide MPAPO protects trigeminal ganglion cell and the retina from hypoxic injury through anti-oxidative stress, anti-apoptosis, and promoting axon regeneration

2021 ◽  
Vol 1865 (12) ◽  
pp. 130018
Author(s):  
Hui-xian Li ◽  
Jia Feng ◽  
Qian Liu ◽  
Bi-qian Ou ◽  
Shi-yin Lu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ganglion Cell ◽  
Trigeminal Ganglion ◽  
Axon Regeneration ◽  
Hypoxic Injury ◽  
Mutant Peptide

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.

Bone Marrow Mononuclear Cells Increase Retinal Ganglion Cell Survival and Axon Regeneration in the Adult Rat

2011 ◽  
Vol 20 (3) ◽  
pp. 391-406 ◽  
Author(s):  
Camila Zaverucha-Do-Valle ◽  
Fernanda Gubert ◽  
Michelle Bargas-Rega ◽  
Juliana L. L. Coronel ◽  
Louise A. Mesentier-Louro ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Ganglion Cell ◽  
Cell Survival ◽  
Retinal Ganglion Cell ◽  
Mononuclear Cells ◽  
Axon Regeneration ◽  
Bone Marrow Mononuclear Cells ◽  
Retinal Ganglion ◽  
Adult Rat ◽  
Retinal Ganglion Cell Survival

scholarly journals Mdivi-1 attenuates oxidative stress and exerts vascular protection in ischemic/hypoxic injury by a mechanism independent of Drp1 GTPase activity

Redox Biology ◽  
2020 ◽  
Vol 37 ◽  
pp. 101706
Author(s):  
Chenyang Duan ◽  
Li Wang ◽  
Jie Zhang ◽  
Xinming Xiang ◽  
Yue Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gtpase Activity ◽  
Vascular Protection ◽  
Hypoxic Injury

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.

Combined retrograde tracing and enzyme/immunohistochemistry of trigeminal ganglion cell bodies innervating tooth pulps in the rat

Neuroscience ◽  
1989 ◽  
Vol 33 (1) ◽  
pp. 101-109 ◽  
Author(s):  
K. Fried ◽  
J. Arvidsson ◽  
B. Robertson ◽  
E. Brodin ◽  
E. Theodorsson
Keyword(s):  
Ganglion Cell ◽  
Trigeminal Ganglion ◽  
Retrograde Tracing
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