BDNF improves axon transportation and rescues visual function in a rodent model of acute elevation of intraocular pressure

Du, Rui; Wang, Xu; He, Shunping

doi:10.1007/s11427-019-1567-0

Cited by 13 publications

(9 citation statements)

References 43 publications

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“…After an IOP rise to ischemic levels in rats, intravitreal injections of the neurotrophic factor BDNF enhanced anterograde and retrograde transport and increased the levels of the motor proteins dynein and kinesin in the optic nerve. This was in parallel to a neuroprotective role of BDNF, also previously described in several models of RGC lesion [ 145 , 146 , 147 , 148 , 149 ]. In line with these studies, the oral delivery of a synthetic anti-inflammatory drug, the sterol derivative HE3286, was able to prevent impairment of anterograde transport in a microbead rat model and ameliorated several aspects of the disease, leading to enhanced levels of BDNF in the retina and the ONH [ 150 ].…”

Section: Neuroprotective Strategies For Glaucomatous Axonopathysupporting

confidence: 78%

The Role of Axonal Transport in Glaucoma

Dias

Luo

Ribas

et al. 2022

IJMS

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Glaucoma is a neurodegenerative disease that affects the retinal ganglion cells (RGCs) and leads to progressive vision loss. The first pathological signs can be seen at the optic nerve head (ONH), the structure where RGC axons leave the retina to compose the optic nerve. Besides damage of the axonal cytoskeleton, axonal transport deficits at the ONH have been described as an important feature of glaucoma. Axonal transport is essential for proper neuronal function, including transport of organelles, synaptic components, vesicles, and neurotrophic factors. Impairment of axonal transport has been related to several neurodegenerative conditions. Studies on axonal transport in glaucoma include analysis in different animal models and in humans, and indicate that its failure happens mainly in the ONH and early in disease progression, preceding axonal and somal degeneration. Thus, a better understanding of the role of axonal transport in glaucoma is not only pivotal to decipher disease mechanisms but could also enable early therapies that might prevent irreversible neuronal damage at an early time point. In this review we present the current evidence of axonal transport impairment in glaucomatous neurodegeneration and summarize the methods employed to evaluate transport in this disease.

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Section: Neuroprotective Strategies For Glaucomatous Axonopathysupporting

confidence: 78%

The Role of Axonal Transport in Glaucoma

Dias

Luo

Ribas

et al. 2022

IJMS

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“…The neuroprotective role of BDNF in the retinal ganglion has been demonstrated in glaucoma animal models. [ 17 , 18 ] The role of BDNF in axon regeneration remains controversial.…”

Section: Discussionmentioning

confidence: 99%

Evaluations of aqueous humor protein markers in different types of glaucoma

et al. 2022

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To compare the concentrations of protein markers in aqueous humor (AH) of patients with primary open-angle glaucoma (POAG), chronic angle-closure glaucoma (CACG), acute primary angle closure (APAC), and cataract without glaucoma as the control group. AH samples were collected at the beginning of surgery from 82 eyes of 82 patients who were divided into POAG (n = 23), CACG (n = 21), APAC (n = 19), and cataract groups (n = 19). The expression levels of interferon-gamma (IFN-γ), interleukin-2 (IL-2), interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin-17A (IL-17A), lymphotoxin-alpha (LT-α), monocyte chemotactic protein-1 (MCP-1), matrix metalloproteinase-2 (MMP-2), brain derived neurotrophic factor (BDNF), basic fibroblast growth factor (bFGF), platelet-derived growth factor-AA (PDGF-AA), vascular endothelial growth factor (VEGF), tissue inhibitor of metalloproteinases-1 (TIMP-1), and tumor necrosis factor-alpha (TNF-α) in AH were detected using a microsphere-based immunoassay. The AH levels of TNF-α, MMP-2, MCP-1, IFN-γ, and TIMP-1 in the APAC and CACG groups were significantly higher than those in control eyes. Additionally, the AH levels of interleukin-6 (IL-6) and VEGF in the APAC group were significantly higher than those in the control group (CG). The interleukin-8 (IL-8) levels in patients with POAG were significantly higher than those in control eyes, whereas the LT-α levels were significantly lower than those in control eyes. IL-6 levels were significantly correlated with the coefficient of variation (CV), whereas IL-6 levels were significantly negatively correlated with the frequency of hexagonal cells (HEX) and corneal endothelial cell density (CD). The levels of TNF-α, MMP-2, MCP-1, IFN-γ, TIMP-1, IL-6, IL-8, VEGF, and LT-α were different among the three types of glaucoma. These different types of glaucoma may be caused by various pathogeneses, which opens avenues for further investigation into the pathogenesis of glaucoma and discoveries new targets and pathways for the treatment of glaucoma.

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“…Neuro-protective strategies could be promising to promote cell survival and prevent retinal neuron death ( Pardue and Allen, 2018 ). Neuroprotective factors, including BDNF, ciliary neurotrophic factor, etc., have considerable potential to act as a powerful neuroprotective agent ( Du et al, 2020 ; Dulz et al, 2020 ). However, significant challenges remain due to short half-lives of these factors and the inability to easily cross the blood brain or blood retina barrier ( Pardue and Allen, 2018 ).…”

Section: Discussionmentioning

confidence: 99%

Stimulation of C-Kit+ Retinal Progenitor Cells by Stem Cell Factor Confers Protection Against Retinal Degeneration

Chen

Liu

et al. 2022

Front. Pharmacol.

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C-kit/CD117, expressed in a series of tissue-specific progenitor cells, plays an important role in tissue regeneration and tissue homeostasis. We previously demonstrated that organoid-derived c-kit+ retinal progenitor cells can facilitate the restoration of degenerated retina. Meanwhile, we have identified a population of endogenous c-kit+ cells in retinas of adult mouse. However, the exact role of these cells in retinal degeneration remains unclear. Here, we demonstrated that stimulation of endogenous c-kit+ cells by stem cell factor (SCF) conferred protection against retinal degeneration. Retinal degeneration was induced by intravitreal injection of N-methyl-D-aspartate (NMDA). NMDA challenge increased the total number of c-kit+ cells in the retinal ganglion cell layer (GCL), while deregulated the protein level of SCF, which was mainly expressed in Müller cells. Both flash electroretinogram (fERG) and light/dark transition tests showed that intravitreal injection of SCF effectively improved the visual function of NMDA-treated mice. Mechanistically, SCF administration not only prevented the loss of retinal ganglion cells (RGCs), but also maintained the function of RGCs as quantified by fERG. Further, we performed transcriptome sequencing analysis of the retinal cells isolated from SCF-treated mice and the parallel control. Gene Ontology analysis showed that SCF-induced transcriptome changes were closely correlated with eye development-related pathways. Crystallins and several protective factors such as Pitx3 were significantly upregulated by SCF treatment. Our results revealed the role of SCF stimulated c-kit+ cells in the protection of RGCs in NMDA-treated mice, via inhibiting the loss of RGCs. Administration of SCF can act as a potent strategy for treating retinal degeneration-related diseases.

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BDNF improves axon transportation and rescues visual function in a rodent model of acute elevation of intraocular pressure

Cited by 13 publications

References 43 publications

The Role of Axonal Transport in Glaucoma

The Role of Axonal Transport in Glaucoma

Evaluations of aqueous humor protein markers in different types of glaucoma

Stimulation of C-Kit+ Retinal Progenitor Cells by Stem Cell Factor Confers Protection Against Retinal Degeneration

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