The Expression Patterns of Nogo-A, Myelin Associated Glycoprotein and Oligodendrocyte Myelin Glycoprotein in the Retina After Ocular Hypertension

Liao, Xinxue; Chen, Dong; Shi, Jianbo; Sun, Yueqi; Sun, Shu-Juan; So, Kwok-Fai; Fu, Qing‐Ling

doi:10.1007/s11064-011-0518-y

Cited by 10 publications

(5 citation statements)

References 38 publications

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“…Silencing Semaphorin 3A enhanced normal vascular regeneration, diminished aberrant neovascularization, and thereby preserved neuroretinal function (69). In a model of ocular hypertension in which the blood supply also is altered, Nogo-A was up-regulated in retinal ganglion cells (71). Therefore, similarly to semaphorins, the increase of Nogo-A at the surface of ischemic neurons may restrict neovascularization in pathological conditions.…”

Section: Discussionmentioning

confidence: 99%

Nogo-A is a negative regulator of CNS angiogenesis

Wälchli

Pernet

Weinmann

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

104

130

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Nogo-A is an important axonal growth inhibitor in the adult and developing CNS. In vitro, Nogo-A has been shown to inhibit migration and cell spreading of neuronal and nonneuronal cell types. Here, we studied in vivo and in vitro effects of Nogo-A on vascular endothelial cells during angiogenesis of the early postnatal brain and retina in which Nogo-A is expressed by many types of neurons. Genetic ablation or virus-mediated knock down of Nogo-A or neutralization of Nogo-A with an antibody caused a marked increase in the blood vessel density in vivo. In culture, Nogo-A inhibited spreading, migration, and sprouting of primary brain microvascular endothelial cells (MVECs) in a dose-dependent manner and induced the retraction of MVEC lamellipodia and filopodia. Mechanistically, we show that only the Nogo-A–specific Delta 20 domain exerts inhibitory effects on MVECs, but the Nogo-66 fragment, an inhibitory domain common to Nogo-A, -B, and -C, does not. Furthermore, the action of Nogo-A Delta 20 on MVECs required the intracellular activation of the Ras homolog gene family, member A (Rho-A)-associated, coiled-coil containing protein kinase (ROCK)-Myosin II pathway. The inhibitory effects of early postnatal brain membranes or cultured neurons on MVECs were relieved significantly by anti–Nogo-A antibodies. These findings identify Nogo-A as an important negative regulator of developmental angiogenesis in the CNS. They may have important implications in CNS pathologies involving angiogenesis such as stroke, brain tumors, and retinopathies.

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Section: Discussionmentioning

confidence: 99%

Nogo-A is a negative regulator of CNS angiogenesis

Wälchli

Pernet

Weinmann

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

104

130

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 88%

“…Oligodendrocyte loss, hypomyelination, and demyelination in different types of neural diseases, including glaucoma, are associated with loss of synapses, dendritic processes, and a lack of protections and supports for normal axonal structures (Faiq et al, 2019; Nakazawa et al, 2006; You et al, 2019). Consequently, these axonal neuropathies will contribute to neuronal death and prolonged neural functional defects (Liao et al, 2011; Renner et al, 2017). In this study, our timeline data detailedly reveals that the increase of OPC numbers in the optic nerves is the first pathological change to occur at the third day in response to glaucoma progression, which can be a reflection of the undetectable demyelination that occurs at the early stage of disease or even reactivation of OPCs.…”

Section: Discussionmentioning

confidence: 99%

Remyelination‐oriented clemastine treatment attenuates neuropathies of optic nerve and retina in glaucoma

Liu,

Yang,

et al. 2024

Glia

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As one of the top causes of blindness worldwide, glaucoma leads to diverse optic neuropathies such as degeneration of retinal ganglion cells (RGCs). It is widely accepted that the level of intraocular pressure (IOP) is a major risk factor in human glaucoma, and reduction of IOP level is the principally most well‐known method to prevent cell death of RGCs. However, clinical studies show that lowering IOP fails to prevent RGC degeneration in the progression of glaucoma. Thus, a comprehensive understanding of glaucoma pathological process is required for developing new therapeutic strategies. In this study, we provide functional and histological evidence showing that optic nerve defects occurred before retina damage in an ocular hypertension glaucoma mouse model, in which oligodendroglial lineage cells were responsible for the subsequent neuropathology. By treatment with clemastine, an Food and Drug Administration (FDA)‐approved first‐generation antihistamine medicine, we demonstrate that the optic nerve and retina damages were attenuated via promoting oligodendrocyte precursor cell (OPC) differentiation and enhancing remyelination. Taken together, our results reveal the timeline of the optic neuropathies in glaucoma and highlight the potential role of oligodendroglial lineage cells playing in its treatment. Clemastine may be used in future clinical applications for demyelination‐associated glaucoma.

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“…IOP elevation may also directly obstruct retinal blood vessels and decrease retinal blood flow ( 36 ). I/R damage of the retina also serves a key role in neuronal cell death in the latter pathological stages ( 37 , 38 ). In the present study, tissue edema and disorder in cell arrangement were observed 1 day after AOH, followed by atrophy of the retina and cell loss 2 days later.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of leukemia inhibitory factor on the retinal injury induced by acute ocular hypertension in rats

Gao

Wang

et al. 2022

Exp Ther Med

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Glaucoma is one of the leading causes of irreversible blindness worldwide. As such, neuroprotective therapy is essential for the treatment of this disease. Leukemia inhibitory factor (LIF) is a member of the IL-6 cytokine family and the LIF signaling pathway is considered to be one of the major endogenous factors mediating neuroprotection in the retina. Therefore, the present study aimed to investigate the possible effects of LIF in acute ocular hypertension (AOH). The intraocular pressure in rat eyes was raised to 110 mmHg for 1 h by infusing the anterior chamber with normal saline to establish the AOH model. In the treatment group, LIF was then injected into the vitreous cavity after AOH was ceased. The retinal tissues were obtained after the termination of AOH, and H&E staining was conducted to assess the morphological damage. The number of retinal ganglion cells (RGCs) was counted using the Fluoro-Gold retrograde staining method. TUNEL staining was used to determine the extent of apoptosis among the retinal cells. In addition, the protein expression levels of cleaved caspase-3, poly (ADP-ribose) polymerase (PARP), STAT3 and components of the AKT/mTOR/70-kDa ribosomal protein S6 kinase (p70S6K) signaling pathway were examined by western blotting. The results showed that AOH induced tissue swelling and structural damage in the retina, which were reversed by LIF injection. In the LIF treatment group, RGC loss was significantly inhibited and the quantity of TUNEL-stained cells was also significantly reduced, whereas the expression of cleaved caspase-3 and PARP was decreased. Furthermore, increased phosphorylation of STAT3, AKT, mTOR and p70S6K was observed after LIF treatment. By contrast, pretreatment with the STAT3 inhibitor C188-9 or the PI3K/AKT/mTOR inhibitor LY3023414 reversed the LIF-induced inhibition of RGC loss. These results suggested that exogenous LIF treatment inhibited the retinal damage induced by AOH, which was associated with the activation of STAT3 and mTOR/p70S6K signaling. Therefore, LIF may serve a role in neuroprotection for glaucoma treatment.

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The Expression Patterns of Nogo-A, Myelin Associated Glycoprotein and Oligodendrocyte Myelin Glycoprotein in the Retina After Ocular Hypertension

Cited by 10 publications

References 38 publications

Nogo-A is a negative regulator of CNS angiogenesis

Nogo-A is a negative regulator of CNS angiogenesis

Remyelination‐oriented clemastine treatment attenuates neuropathies of optic nerve and retina in glaucoma

Protective effect of leukemia inhibitory factor on the retinal injury induced by acute ocular hypertension in rats

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