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Tppp3 acts as a new therapeutic gene for optic nerve regeneration

ABSTRACT: In this study, we investigated the role of Tppp3 overexpression on axon regeneration and RGC survival in a mouse optic nerve crush model. We observed that Tppp3 overexpression upregulates expression levels of axon regeneration-induced genes and cellular pathways, such as BMP4 and neuroinflammation, thereby resulting in improved RGC survival and axon regeneration.

ORGANISM(S): Mus musculus

PROVIDER: GSE241230 | GEO | 2025/02/01

REPOSITORIES: GEO

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Aldose reductase inhibition decelerates optic nerve degeneration by suppressing retinal microglia activation

Project description:To investigate the role of aldose reductase (AR) inhibition using Sorbinil on retinal microglia (RMG) activation, retinal ganglion cell (RGC) survival, and axon regeneration after optic nerve trauma. We observed that AR inhibition using Sorbinil attenuates RMG activation and subsequently promotes RGC survival and delays axon degeneration one week after optic nerve crush.

2023-04-05 | GSE200233 | GEO

Immunomodulation by the combination of statin and matrix-bound nanovesicle enhances optic nerve regeneration

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2024-06-05 | GSE226780 | GEO

Retinal Ly6Clow Mo/MΦ protect optic nerve against injury

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Project description:Retinal ganglion cell (RGC) death is the final consequence of many blinding diseases, where there is considerable variation in the time course and severity of RGC loss. Indeed, this process appears to be influenced by a wide variety of genetic and environmental factors. In this study we explored the genetic basis for differences in ganglion cell death in two inbred strains of mice. We found that RGCs are more susceptible to death following optic nerve crush in C57BL/6J mice (54% survival) than in DBA2/J mice (62% survival). Using the Illumina Mouse-6 microarray, we identified 1,580 genes with significant change in expression following optic nerve crush in these two strains of mice. Our analysis of the changes occurring after optic nerve crush demonstrated that the greatest amount of change (44% of the variance) was due to the injury itself. This included changes associated with ganglion cell death, reactive gliosis, and abortive regeneration. The second pattern of gene changes (23% of the variance) was primarily related to differences in gene expressions observed between the C57BL/6J and DBA/2J mouse strains. The remaining changes in gene expression represent interactions between the effects of optic nerve crush and the genetic background of the mouse. We extracted one genetic network from this dataset that appears to be related to tissue remodeling. One of the most intriguing sets of changes included members of the crystallin family of genes, which may represent a signature of pathways modulating the susceptibility of cells to death. Differential responses to optic nerve crush between two widely used strains of mice were used to define molecular networks associated with ganglion cell death and reactive gliosis. These results form the basis for our continuing interest in the modifiers of retinal injury. 18 Samples: 9 per strain (C57BL/6J & DBA/2J); 3 conditions per strain

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Single nuclei RNA-seq analysis of control and Dnmt3a conditional knockout (cKO) of retinal ganglion cells at 2 days post optic nerve crush.

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