Hypoxia augments TNF-$alpha;-mediated endothelin-1 release and cell proliferation in human optic nerve head astrocytes

Desai, Devashish H.

doi:10.1016/s0006-291x(04)00806-x

Cited by 18 publications

(24 citation statements)

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“…The ONH damage explains the bundleshaped damage and loss of retinal ganglion cells and their axons [107]. Hypoxia (e.g., by varying blood supply in FS) in the retina induces ET-1 production mainly by unoxidized hypoxia-induced transcription factor 1α (HIF-1α) that serves as a Bmaster switch^ [119] that activates (among others) transcription of ET-1 and VEGF [120].…”

Section: Endothelial Dysregulation In Flammer Syndromementioning

confidence: 99%

Endothelial dysfunction in cardiovascular disease and Flammer syndrome—similarities and differences

et al. 2017

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The endothelium has increasingly been recognized as a smart barrier and a key regulator of blood flow in microand macrovascular beds. Endothelial dysfunction marks a stage of atherosclerosis and is an important prognostic marker for cardiovascular disease. Yet, some people who tend to be slim and physically active and with rather low blood pressure show a propensity to respond to certain stimuli such as emotional stress with endothelial-mediated vascular dysregulation (Flammer syndrome). This leads to characteristic vascular symptoms such as cold hands but also a risk for vascularmediated diseases such as normal-tension glaucoma. It is the aim of this review to delineate the differences between Flammer syndrome and its Bcounterpart^endothelial dysfunction in the context of cardiovascular diseases.

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Section: Endothelial Dysregulation In Flammer Syndromementioning

confidence: 99%

Endothelial dysfunction in cardiovascular disease and Flammer syndrome—similarities and differences

et al. 2017

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“…TNF-α is a potent stimulator of ET-1 synthesis and secretion in several ocular cell types, including optic nerve head astrocytes (Desai et al, 2004).…”

Section: Interplay Of Tnf-α Signaling With Other Cellular Events Assomentioning

confidence: 99%

TNF-α signaling in glaucomatous neurodegeneration

Tezel

2008

Progress in Brain Research

237

190

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Growing evidence supports the role of TNF-α as a mediator of neurodegeneration in glaucoma. Glial production of TNF-α is increased and its death receptor is up-regulated on retinal ganglion cells (RGCs) and optic nerve axons in glaucomatous eyes. This multifunctional cytokine can induce RGC death through receptor-mediated caspase activation, mitochondrial dysfunction, and oxidative stress. Opposing these cell-death promoting signals, binding of TNF receptors can also trigger the activation of survival signals. A critical balance between a variety of intracellular signaling pathways determines the predominant in vivo bioactivity of TNF-α as best exemplified by differential responses of RGCs and glia. In addition to the direct neurotoxicity of TNF-α to RGCs and their axons, potential interplay of TNF-α signaling with other cellular events associated with glaucomatous neurodegeneration may also contribute to secondary neurodegenerative injury. This review focuses on the present evidence supporting the involvement of TNF-α signaling in glaucomatous neurodegeneration and possible treatment targets to provide neuroprotection.

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“…Expression of ET-1 and its receptors (ET-Rs) is strongly upregulated in astrocytes after brain injury (Jiang et al, 1993;Zhang et al, 1994;Hino et al, 1996;Nie and Olsson, 1996;Rogers et al, 1997;Sakurai-Yamashita et al, 1997;Baba, 1998). Astrocytes are autocrine targets of ET-1 action, which results in increased cell proliferation (Lazarini et al, 1996;Hasselblatt et al, 2001Hasselblatt et al, , 2003Rogers et al, 2003;Desai et al, 2004). A direct role for ET-1 in reactive gliosis was demonstrated by in vivo infusion of exogenous ETs or ET-R agonists, which caused astrocyte hypertrophy and proliferation .…”

Section: Introductionmentioning

confidence: 99%

Endothelin-1 Regulates Astrocyte Proliferation and Reactive Gliosis via a JNK/c-Jun Signaling Pathway

Gadea¹,

Schinelli²,

Gallo³

2008

J. Neurosci.

225

191

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Hypoxia augments TNF-$alpha;-mediated endothelin-1 release and cell proliferation in human optic nerve head astrocytes

Cited by 18 publications

References 0 publications

Endothelial dysfunction in cardiovascular disease and Flammer syndrome—similarities and differences

Endothelial dysfunction in cardiovascular disease and Flammer syndrome—similarities and differences

TNF-α signaling in glaucomatous neurodegeneration

Endothelin-1 Regulates Astrocyte Proliferation and Reactive Gliosis via a JNK/c-Jun Signaling Pathway

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