scholarly journals Knocking out non-muscle myosin II in retinal ganglion cells promotes long-distance optic nerve regeneration

2019 ◽  
Author(s):  
Xue-Wei Wang ◽  
Shu-Guang Yang ◽  
Chi Zhang ◽  
Jin-Jin Ma ◽  
Yingchi Zhang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Optic Nerve ◽  
Retinal Ganglion Cells ◽  
Axon Regeneration ◽  
Ganglion Cells ◽  
Myosin Ii ◽  
Retinal Ganglion ◽  
Long Distance ◽  
Optic Nerve Regeneration ◽  
Cytoskeletal Dynamics

AbstractIn addition to altered gene expression, pathological cytoskeletal dynamics in the axon are another key intrinsic barrier for axon regeneration in the central nervous system (CNS). Here we showed that knocking out myosin IIA/B in retinal ganglion cells alone either before or after optic nerve crush induced marked and sustained optic nerve regeneration. Combined Lin28 overexpression and myosin IIA/B knockout led to synergistic promoting effect and long-distance axon regeneration. Immunostaining, RNA-seq and western blot analyses revealed that myosin II deletion did not affect known axon regeneration signaling pathways or the expression of regeneration associated genes. Instead, it abolished the retraction bulb formation and significantly enhanced the axon extension efficiency. The study provided clear evidence that directly targeting neuronal cytoskeleton was sufficient to induce strong CNS axon regeneration, and combining gene expression in the soma and modified cytoskeletal dynamics in the axon was a promising approach for long-distance CNS axon regeneration.

scholarly journals Knocking Out Non-muscle Myosin II in Retinal Ganglion Cells Promotes Long-Distance Optic Nerve Regeneration

Cell Reports ◽  
2020 ◽  
Vol 31 (3) ◽  
pp. 107537 ◽  
Author(s):  
Xue-Wei Wang ◽  
Shu-Guang Yang ◽  
Chi Zhang ◽  
Ming-Wen Hu ◽  
Jiang Qian ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Nerve Regeneration ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Myosin Ii ◽  
Retinal Ganglion ◽  
Long Distance ◽  
Optic Nerve Regeneration ◽  
Muscle Myosin

scholarly journals Retinal Ganglion Cells Downregulate Gene Expression and Lose Their Axons within the Optic Nerve Head in a Mouse Glaucoma Model

2008 ◽  
Vol 28 (2) ◽  
pp. 548-561 ◽  
Author(s):  
I. Soto ◽  
E. Oglesby ◽  
B. P. Buckingham ◽  
J. L. Son ◽  
E. D. O. Roberson ◽  
...  
Keyword(s):  
Gene Expression ◽  
Optic Nerve ◽  
Retinal Ganglion Cells ◽  
Optic Nerve Head ◽  
Ganglion Cells ◽  
Retinal Ganglion

scholarly journals Upregulation of IGF-I in the goldfish retinal ganglion cells during the early stage of optic nerve regeneration

2007 ◽  
Vol 50 (5) ◽  
pp. 749-756 ◽  
Author(s):  
Yoshiki Koriyama ◽  
Keiko Homma ◽  
Kayo Sugitani ◽  
Yoshihiro Higuchi ◽  
Toru Matsukawa ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Nerve Regeneration ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Early Stage ◽  
Retinal Ganglion ◽  
Optic Nerve Regeneration ◽  
Igf I

scholarly journals Changes in axonally transported proteins during axon regeneration in toad retinal ganglion cells.

1981 ◽  
Vol 89 (1) ◽  
pp. 86-95 ◽  
Author(s):  
J H Skene ◽  
M Willard
Keyword(s):  
Optic Nerve ◽  
Retinal Ganglion Cells ◽  
Axon Regeneration ◽  
Ganglion Cells ◽  
Small Subset ◽  
Retinal Ganglion ◽  
Radioactive Label ◽  
Altered Expression ◽  
Growth State ◽  
Mature Neuron

In an effort to understand the regulation of the transition of a mature neuron to the growth, or regenerating, state we have analyzed the composition of the axonally transported proteins in the retinal ganglion cells of the toad Bufo marinus after inducing axon regeneration by crushing the optic nerve. At increasing intervals after axotomy, we labeled the retinal ganglion cells with [35S]methionine and subsequently analyzed the labeled transported polypeptides in the crushed optic nerve by means of one- and two-dimensional electrophoretic techniques. The most significant conclusion from these experiments is that, while the transition from the mature to the regenerating state does not require a gross qualitative alteration in the composition of axonally transported proteins, the relative labeling of a small subset of rapidly transported proteins is altered dramatically (changes of more than 20-fold) and reproducibly (more than 30 animals) by axotomy. One of these growth-associated proteins (GAPs) was soluble in an aqueous buffer, while three were associated with a crude membrane fraction. The labeling of all three of the membrane-associated GAPs increased during the first 8 d after axotomy, and they continued to be labeled for at least 4 wk. The modulation of these proteins after axotomy is consistent with the possibility that they are involve in growth-specific functions and that the altered expression of a small number of genes is a crucial regulatory event in the transition of a mature neuron to a growth state. In addition to these selective changes in rapidly transported proteins, we observed the following more general metabolic correlates of the regeneration process: The total radioactive label associated with the most rapidly transported proteins (groups I and II) increased three to fourfold during the first 8 d after the nerve was crushed, while the total label associated with more slowly moving proteins (group IV) increased about 10-fold during this same period. Among these more slowly transported polypeptides, five were observed whose labeling increased much more than the average. Three of these five polypeptides resemble actin and alpha- and beta-tubulin in their electrophoretic properties.

scholarly journals Harnessing Astrocytes and Müller Glial Cells in the Retina for Survival and Regeneration of Retinal Ganglion Cells

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1339
Author(s):  
Hyung-Suk Yoo ◽  
Ushananthini Shanmugalingam ◽  
Patrice D. Smith
Keyword(s):  
Spinal Cord ◽  
Optic Nerve ◽  
Retinal Ganglion Cells ◽  
Axon Regeneration ◽  
Ganglion Cells ◽  
Reactive Gliosis ◽  
Retinal Ganglion ◽  
Cord Injury ◽  
The Central Nervous System ◽  
Retinal Degenerative Diseases

Astrocytes have been associated with the failure of axon regeneration in the central nervous system (CNS), as it undergoes reactive gliosis in response to damages to the CNS and functions as a chemical and physical barrier to axon regeneration. However, beneficial roles of astrocytes have been extensively studied in the spinal cord over the years, and a growing body of evidence now suggests that inducing astrocytes to become more growth-supportive can promote axon regeneration after spinal cord injury (SCI). In retina, astrocytes and Müller cells are known to undergo reactive gliosis after damage to retina and/or optic nerve and are hypothesized to be either detrimental or beneficial to survival and axon regeneration of retinal ganglion cells (RGCs). Whether they can be induced to become more growth-supportive after retinal and optic nerve injury has yet to be determined. In this review, we pinpoint the potential molecular pathways involved in the induction of growth-supportive astrocytes in the spinal cord and suggest that stimulating the activation of these pathways in the retina could represent a new therapeutic approach to promoting survival and axon regeneration of RGCs in retinal degenerative diseases.

Sign in / Sign up

Export Citation Format

Share Document