scholarly journals Longitudinal In Vivo Changes in Retinal Ganglion Cell Dendritic Morphology After Acute and Chronic Optic Nerve Injury

2021 ◽  
Vol 62 (9) ◽  
pp. 5
Author(s):  
Delaney C. M. Henderson ◽  
Jayme R. Vianna ◽  
John Gobran ◽  
Johnny Di Pierdomenico ◽  
Michele L. Hooper ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Ganglion Cell ◽  
Nerve Injury ◽  
Retinal Ganglion Cell ◽  
Dendritic Morphology ◽  
Retinal Ganglion ◽  
Optic Nerve Injury

scholarly journals Retinal ganglion cell survival after severe optic nerve injury is modulated by crosstalk between JAK/STAT signaling and innate immune responses in the zebrafish retina

Development ◽  
2021 ◽  
Author(s):  
Si Chen ◽  
Kira L. Lathrop ◽  
Takaaki Kuwajima ◽  
Jeffrey M. Gross
Keyword(s):  
Optic Nerve ◽  
Immune Responses ◽  
Ganglion Cell ◽  
Nerve Injury ◽  
Retinal Ganglion Cell ◽  
Visual Information ◽  
Retinal Ganglion ◽  
Optic Nerve Injury ◽  
Pathway Activity ◽  
Stat Pathway

Visual information is transmitted from the eye to the brain along the optic nerve, a structure composed of retinal ganglion cell (RGC) axons. The optic nerve is highly vulnerable to damage in neurodegenerative diseases like glaucoma and there are currently no FDA-approved drugs or therapies to protect RGCs from death. Zebrafish possess remarkable neuroprotective and regenerative abilities and here, utilizing an optic nerve transection (ONT) injury and an RNA-seq-based approach, we identify genes and pathways active in RGCs that may modulate their survival. Through pharmacological perturbation, we demonstrate that JAK/STAT pathway activity is required for RGC survival after ONT. Furthermore, we show that immune responses directly contribute to RGC death after ONT; macrophages/microglia are recruited to the retina and blocking neuroinflammation or depleting these cells after ONT rescues survival of RGCs. Taken together, these data support a model in which crosstalk between macrophages/microglia and RGCs, mediated by Jak/Stat pathway activity, regulates RGC survival after optic nerve injury.

scholarly journals Aerobic exercise delays retinal ganglion cell death after optic nerve injury

2020 ◽  
Vol 200 ◽  
pp. 108240
Author(s):  
Yuan-Yuan He ◽  
Lu Wang ◽  
Tao Zhang ◽  
Shi-Jun Weng ◽  
Jian Lu ◽  
...  
Keyword(s):  
Cell Death ◽  
Optic Nerve ◽  
Aerobic Exercise ◽  
Ganglion Cell ◽  
Nerve Injury ◽  
Retinal Ganglion Cell ◽  
Retinal Ganglion ◽  
Optic Nerve Injury ◽  
Retinal Ganglion Cell Death ◽  
Ganglion Cell Death

Carvedilol Promotes Retinal Ganglion Cell Survival Following Optic Nerve Injury via ASK1-p38 MAPK Pathway

2020 ◽  
Vol 18 (9) ◽  
pp. 695-704 ◽  
Author(s):  
Bei Liu ◽  
Yu-Jia Liu
Keyword(s):  
Optic Nerve ◽  
Ganglion Cell ◽  
Nerve Injury ◽  
Retinal Ganglion Cell ◽  
Mapk Pathway ◽  
Mitogen Activated Protein Kinase ◽  
Ganglion Cell Complex ◽  
Retinal Layer ◽  
Retinal Ganglion ◽  
Optic Nerve Injury

Background: Carvedilol, which is considered as a nonselective β-adrenoreceptor blocker, has many pleiotropic activities. It also causes great impact on neuroprotection because of its antioxidant ability, which suggested that carvedilol may be effective in protecting RGCs from increased oxidative stress. Objective: To examine the effects of carvedilol on preventing Retinal Ganglion Cell (RGC) death in a mouse model of Optic Nerve Injury (ONI). Methods: C57BL/6J mice were subjected to Optic Nerve Injury (ONI) model and treated with carvedilol or placebo. Histological and morphometric studies were performed; the RGC number, the amount of neurons in the ganglion cell layer and the thickness of the Inner Retinal Layer (IRL) was quantified. The average thickness of Ganglion Cell Complex (GCC) was determined by the Spectral- Domain OCT (SD-OCT) assay. Immunohistochemistry, western blot and quantitative real-time PCR analysis were also applied. Results: Daily treatment of carvedilol reduced RGC death following ONI, and in vivo retinal imaging revealed that carvedilol can effectively prevent retinal degeneration. The expression of chemokines important for micorglia recruitment was deceased with carvedilol ingestion and the accumulation of retinal microglia is reduced consequently. In addition, the ONI-induced expression of inducible nitric oxide synthase in the retina was inhibited with carvedilol treatment in the retina. We also discovered that carvedilol suppressed ONI-induced activation of Apoptosis Signal-regulating Kinase-1 (ASK1) and p38 Mitogen-Activated Protein Kinase (MAPK) pathway. Conclusion: The results of this study indicate that carvedilol can stimulate neuroprotection and neuroregeneration, and may be useful for treatment of various neurodegenerative diseases.

Apoptotic Versus Necrotic Characteristics of Retinal Ganglion Cell Death After Partial Optic Nerve Injury

1999 ◽  
Vol 16 (2) ◽  
pp. 153-163 ◽  
Author(s):  
ANNETT BIEN ◽  
CONSTANZE I. SEIDENBECHER ◽  
TOBIAS M. BÖCKERS ◽  
BERNHARD A. SABEL ◽  
MICHAEL R. KREUTZ
Keyword(s):  
Cell Death ◽  
Optic Nerve ◽  
Ganglion Cell ◽  
Nerve Injury ◽  
Retinal Ganglion Cell ◽  
Retinal Ganglion ◽  
Optic Nerve Injury ◽  
Retinal Ganglion Cell Death ◽  
Ganglion Cell Death

scholarly journals Semaphorin3A increases M1-like microglia and retinal ganglion cell apoptosis after optic nerve injury

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Liu Yun-Jia ◽  
Chen Xi ◽  
Zhang Jie-Qiong ◽  
Zhu Jing-Yi ◽  
Lin Sen ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Ganglion Cell ◽  
Nerve Injury ◽  
Retinal Ganglion Cell ◽  
Microglial Activation ◽  
Current Evidence ◽  
Retinal Ganglion ◽  
Optic Nerve Injury ◽  
Activation Markers ◽  
Continuous Increase

Abstract Background The mechanisms leading to retinal ganglion cell (RGC) death after optic nerve injury have not been fully elucidated. Current evidence indicates that microglial activation and M1- and M2-like dynamics may be an important factor in RGC apoptosis after optic nerve crush (ONC). Semaphorin3A (Sema3A) is a classic axonal guidance protein,which has been found to have a role in neuroinflammation processes. In this study, we investigated the contribution of microglial-derived Sema3A to progressive RGC apoptosis through regulating paradigm of M1- and M2-like microglia after ONC. Method A mouse ONC model and a primary microglial-RGC co-culture system were used in the present study. The expression of M1- and M2-like microglial activation markers were assessed by real-time polymerase chain reaction (RT-qPCR). Histological and Western blot (WB) analyses were used to investigate the polarization patterns of microglia transitions and the levels of Sema3A. RGC apoptosis was investigated by TUNEL staining and caspase-3 detection. Results Levels of Sema3A in the mouse retina increased after ONC. Treatment of mice with the stimulating factor 1 receptor antagonist PLX3397 resulted in a decrease of retinal microglia. The levels of CD16/32 (M1) were up-regulated at days 3 and 7 post-ONC. However, CD206 (M2) declined on day 7 after ONC. Exposure to anti-Sema3A antibodies (anti-Sema3A) resulted in a decrease in the number of M1-like microglia, an increase in the number of M2-like microglia, and the amelioration of RGC apoptosis. Conclusions An increase in microglia-derived Sema3A in the retina after ONC partially leads to a continuous increase of M1-like microglia and plays an important role in RGC apoptosis. Inhibition of Sema3A activity may be a novel approach to the prevention of RGC apoptosis after optic nerve injury.

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