Exploring the role of DLK in the retinal ganglion cell response to optic nerve injuries

Author(s):  
Yiren Zhou
2017 ◽  
Vol 426 (2) ◽  
pp. 360-373 ◽  
Author(s):  
G.B. Whitworth ◽  
B.C. Misaghi ◽  
D.M. Rosenthal ◽  
E.A. Mills ◽  
D.J. Heinen ◽  
...  

2017 ◽  
Vol 162 ◽  
pp. 97-103 ◽  
Author(s):  
Zhen Puyang ◽  
Hai-Qing Gong ◽  
Shi-Gang He ◽  
John B. Troy ◽  
Xiaorong Liu ◽  
...  

2018 ◽  
Vol 59 (3) ◽  
pp. 1562 ◽  
Author(s):  
Min H. Kang ◽  
Mengchen Suo ◽  
Chandrakumar Balaratnasingam ◽  
Paula K. Yu ◽  
William H. Morgan ◽  
...  

2015 ◽  
Vol 56 (10) ◽  
pp. 6095 ◽  
Author(s):  
Francisco M. Nadal-Nicolás ◽  
Paloma Sobrado-Calvo ◽  
Manuel Jiménez-López ◽  
Manuel Vidal-Sanz ◽  
Marta Agudo-Barriuso

Author(s):  
Tian Wang ◽  
Yiming Li ◽  
Miao Guo ◽  
Xue Dong ◽  
Mengyu Liao ◽  
...  

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.


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