retinal degeneration/хипоксия

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Perinatal hypoxia induces subsequent retinal degeneration in the offspring of ovoviviparous fish, Xiphophorous maculates.

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OBJECTIVE This experiment evaluated the perinatal hypoxic effect on the retina of offspring of the ovoviviparous fish. METHODS The ovoviviparous fish Xiphophorous maculates was used for the experiment. METHODS The mothers were kept in a hypoxic environment of 3.5% oxygen for 6 h, starting 30 h

Exacerbation of retinal degeneration in the absence of alpha crystallins in an in vivo model of chemically induced hypoxia.

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This study evaluated the role of crystallins in retinal degeneration induced by chemical hypoxia. Wild-type, alphaA-crystallin (-/-), and alphaB-crystallin (-/-) mice received intravitreal injection of 12 nmol (low dose), 33 nmol (intermediate dose) or 60 nmol (high dose) cobalt chloride (CoCl(2)).

Protective role of somatostatin receptor 2 against retinal degeneration in response to hypoxia.

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In mouse retinal explants, octreotide, a somatostatin [somatotropin release-inhibiting factor (SRIF)] receptor 2 (sst(2)) agonist, prevents the hypoxia-induced vascular endothelial growth factor upregulation. In mice with oxygen-induced retinopathy (OIR), a model of retinopathy of prematurity,

Chlorogenic acid and coffee prevent hypoxia-induced retinal degeneration.

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This study explored whether chlorogenic acid (CGA) and coffee have protective effects against retinal degeneration. Under hypoxic conditions, the viability of transformed retinal ganglion (RGC-5) cells was significantly reduced by treatment with the nitric oxide (NO) donor

Normoxic activation of hypoxia-inducible factors in photoreceptors provides transient protection against light-induced retinal degeneration.

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OBJECTIVE Hypoxic preconditioning activates hypoxia-inducible transcription factors (HIFs) in the retina and protects photoreceptors from light-induced retinal degeneration. The authors tested whether photoreceptor-specific activation of HIFs in normoxia is sufficient for

Retina-specific activation of a sustained hypoxia-like response leads to severe retinal degeneration and loss of vision.

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Loss of vision and blindness in human patients is often caused by the degeneration of neuronal cells in the retina. In mouse models, photoreceptors can be protected from death by hypoxic preconditioning. Preconditioning in low oxygen stabilizes and activates hypoxia inducible transcription factors

Protective role of endogenous PACAP in inflammation-induced retinal degeneration.

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OBJECTIVE Pituitary adenylate cyclase activating polypeptide (PACAP) is a neuroprotective peptide that has been shown to exert protective effects in different models of neurodegenerative diseases, including retinal degenerations. Data obtained from PACAP-deficient (PACAP KO) mice provide evidence

A new model of retinal photoreceptor cell degeneration induced by a chemical hypoxia-mimicking agent, cobalt chloride.

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Retinal photoreceptor cell degeneration was induced by cobalt chloride, a chemical hypoxia-mimicking agent in rodents. Time course and dose-response of photoreceptor cell degeneration in mouse retina after intravitreal injection of cobalt chloride were examined by conventional histological analysis

Involvement of calpain isoforms in retinal degeneration in WBN/Kob rats.

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Results of our recent studies in rats suggested that calpains play an important role in retinal cell death induced by ischemia-reperfusion in vivo and by hypoxia in vitro. Study of spontaneous animal models could help determine the involvement of calpains in human retinopathy. The WBN/Kob rat is

Hypoxia induces beta-amyloid in association with death of RGC-5 cells in culture.

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Beta-amyloid (Aβ) derived from amyloid precursor protein (APP) has been associated with retinal degeneration in Alzheimer's disease (AD) and glaucoma. This study examined whether hypoxia exposure induces Aβ accumulation in RGC-5 cells. While levels of APP mRNA and protein significantly increased in

Effects of phenolic acid metabolites formed after chlorogenic acid consumption on retinal degeneration in vivo.

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METHODS Although ingestion of coffee and its constituent chlorogenic acid (CGA) protects the retina from oxidative stress, the bioaccessibility and bioavailability of coffee metabolites are not well understood. The aim of this study was to determine which coffee metabolites reach the retina and

Ceruloplasmin alters intracellular iron regulated proteins and pathways: ferritin, transferrin receptor, glutamate and hypoxia-inducible factor-1α.

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Ceruloplasmin (Cp) is a ferroxidase important to the regulation of both systemic and intracellular iron levels. Cp has a critical role in iron metabolism in the brain and retina as shown in patients with aceruloplasminemia and in Cp-/-hep-/y mice where iron accumulates and neural and retinal

The role of the hypoxia response in shaping retinal vascular development in the absence of Norrin/Frizzled4 signaling.

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OBJECTIVE To define the role of hypoxia and vascular endothelial growth factor (VEGF) in modifying the pattern, density, and permeability of the retinal vasculature in mouse models in which Norrin/Frizzled4 signaling is impaired. METHODS Retinal vascular structure was analyzed in mice with mutation

Purinergic signaling in retinal degeneration and regeneration.

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Purinergic signaling is centrally involved in mediating the degeneration of the injured and diseased retina, the induction of retinal gliosis, and the protection of the retinal tissue from degeneration. Dysregulated calcium signaling triggered by overactivation of P2X7 receptors is a crucial step in

Retinal degeneration and local oxygen metabolism.

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Vision loss due to various forms of outer retinal degeneration remains a major problem in clinical ophthalmology. Most retinal degenerations are precipitated by genetic mutations affecting the retinal pigment epithelium and sensory retina, but it is becoming increasingly evident that resultant

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