Longitudinal in vivo evaluation of retinal ganglion cell complex layer and dendrites in mice with experimental autoimmune encephalomyelitis

Qian, Zhen; Zheng, Ke; Xu, Yanxuan; Chen, Si; Chen, Shaowan; Liang, Jiajian; Cao, Yingjie; Ng, Tsz Kin; Qiu, Kunliang

doi:10.1016/j.exer.2023.109708

Experimental Eye Research

2023

DOI: 10.1016/j.exer.2023.109708

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Longitudinal in vivo evaluation of retinal ganglion cell complex layer and dendrites in mice with experimental autoimmune encephalomyelitis

Zhen Qian,

Ke Zheng,

Yanxuan Xu

et al.

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2024

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Cellular senescence mediates retinal ganglion cell survival regulation post‐optic nerve crush injury

Yao,

Bin,

et al. 2024

Cell Proliferation

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Traumatic optic neuropathy refers to optic nerve (ON) injury by trauma, including explosion and traffic accident. Retinal ganglion cell (RGC) death is the critical pathological cause of irreversible visual impairment and blindness in ON injury. We previously investigated the patterns of 11 modes of cell death in mouse retina post‐ON injury. Here we aimed to identify additional signalling pathways regulating RGC survival in rodents post‐ON injury. RNA sequencing analysis identified the upregulation of inflammation and cellular senescence‐related genes in retina post‐ON injury, which were confirmed by immunoblotting and immunofluorescence analyses. Increased expression of senescence‐associated β‐galactosidase (SA‐βgal) in RGCs and activation of microglia were also found. Transforming growth factor‐β receptor type II inhibitor (LY2109761) treatment suppressed p15Ink4b and p21Cip1 protein and SA‐βgal expression and promoted RGC survival post‐ON injury with decreasing the expression of cell death markers in retina. Consistently, senolytics (dasatinib and quercetin) treatments can promote RGC survival and alleviate the reduction of ganglion cell complex thickness and pattern electroretinography activity post‐ON injury with reducing SA‐βgal, p15Ink4b, p21Cip1, microglial activation and cell death marker expression. In summary, this study revealed the activation of cellular senescence in rodent retina post‐ON injury and contribute to RGC survival regulation. Targeting cellular senescence can promote RGC survival after ON injury, suggesting a potential treatment strategy for traumatic optic neuropathy.

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Cellular senescence mediates retinal ganglion cell survival regulation post‐optic nerve crush injury

Yao,

Bin,

et al. 2024

Cell Proliferation

View full text Add to dashboard Cite

show abstract

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Longitudinal in vivo evaluation of retinal ganglion cell complex layer and dendrites in mice with experimental autoimmune encephalomyelitis

Cited by 1 publication

References 33 publications

Cellular senescence mediates retinal ganglion cell survival regulation post‐optic nerve crush injury

Cellular senescence mediates retinal ganglion cell survival regulation post‐optic nerve crush injury

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