The Experts below are selected from a list of 195 Experts worldwide ranked by ideXlab platform
Pei-chang Wu - One of the best experts on this subject based on the ideXlab platform.
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The upregulation of zinc finger protein 670 and Prostaglandin D2 synthase in proliferative vitreoretinopathy
Graefe's Archive for Clinical and Experimental Ophthalmology, 2016Co-Authors: Yi-hao Chen, Yi-chan Wu, Faye Huang, Jentaie Shiea, Pei-chang WuAbstract:Purpose Proteins in the vitreous play an important role on the induction of proliferative vitreoretinopathy (PVR) after retinal detachment. The aim of this study was to investigate the variation of protein patterns in the vitreous of PVR eyes and examine whether differentially expressed protein levels were expressed in experimental PVR retina. Methods Vitreous samples from PVR and macular hole patients were selected for proteomic analysis. The vitreous protein samples were separated by two-dimensional electrophoresis (2-DE). The differentially expressed protein spots in the two groups were excised and subjected to in-gel digestion and identification by electrospray ionization mass spectrometry (ESI-MS) analysis. Two differentially expressed proteins, zinc finger protein 670 (ZFP 670) and Prostaglandin D2 synthase (PGD2S), were further validated by immunohistochemical staining and western blotting analysis in the retina of the experimental rabbit PVR model. Results In proteome analysis of human vitreous samples, five proteins had increased expression in PVR, including zinc finger protein 670 (ZFP 670), Prostaglandin D2 synthase (PGD2S), IgG (Immunoglobulin G) light chain, transthyretin precursor, and haptoglobin precursor. ZFP 670 and PGD2S levels were expressed significantly higher in the experimental PVR retinas than in the control group. Conclusions Levels of ZFP 670 and PGD2S were elevated in the vitreous fluid of patients with PVR. In addition, there were higher expressions of ZFP 670 and PGD2S in the experimental PVR retina. This result will expand our knowledge of pathophysiologic characteristics of PVR, and might be helpful for further developing possible treatment on this disorder.
Osamu Hayaishi - One of the best experts on this subject based on the ideXlab platform.
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Specificity of Prostaglandin D2 binding to synaptic membrane fraction of rat brain.
Brain Research, 2003Co-Authors: Hidekado Tokumoto, Yasuyoshi Watanabe, Akira Yamashita, Yoshinobu Arai, Osamu HayaishiAbstract:Abstract The structural requirement of the Prostaglandin D2 molecule for binding to the synaptic membrane fraction of rat brain was extensively studied by using various Prostaglandin D derivatives. Most strict specificity was found in the structures of the cyclo-pentane ring and the double bond in 13,14-position. The addition and deprivation of the double bond in α- and ω-chain, except on 13,14-position, moderately affected the binding. The modification in the car☐yl terminus and ω-chain terminus did not seriously influence the binding. BW 245C and 9-β-Prostaglandin D2, potent agonists for the Prostaglandin D2 receptor in the platelet membrane, were almost ineffective. [3H]Prostaglandin D2 binding was not affected by the addition of various neuroactive substances to the binding assay mixture. Further, Prostaglandin D2 did not affect the known neurotransmitter receptor bindings in the rat brain.
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Strong rebound of wakefulness follows Prostaglandin D2- or adenosine A2a receptor agonist-induced sleep.
Journal of Sleep Research, 2000Co-Authors: Dmitry Gerashchenko, Yoshihiro Urade, Yasuhisa Okano, Shojiro Inoué, Osamu HayaishiAbstract:SUMMARY We studied the effect of sleep excess on the sleep-wakefulness pattern of rats. Subarachnoid infusion of Prostaglandin D2 or the adenosine A2a receptor agonist CGS21680 effectively induced slow wave sleep (SWS) for the first 12 h of the night-time period, whereas they did not induce sleep during the following 24 h of infusion. An increase in the amount of wakefulness was seen during the last 12 h of Prostaglandin D2 infusion. The amounts of wakefulness strongly increased during the following 36-h recovery period. Rebound wakefulness was extraordinarily strong after the cessation of CGS21680 infusion, reaching almost complete insomnia during the night-time. Treatment of animals with Prostaglandin D2 overnight, following by treatment with CGS21680 on the next night, resulted in the strongest induction of wakefulness rebound. During the rebound period, the amount of wakefulness reached up to 50 min per hour in the daytime. Rebound of wakefulness depended on the amounts of preceding SWS induced by infusion of Prostaglandin D2 for 6 or 12 h and of CGS21680 for 12 h. The larger the amount of SWS, the larger the amount of the following rebound of wakefulness. Rebounds of wakefulness occurred as a result of decrease in SWS amounts, whereas paradoxical sleep amounts did not change. Desensitization of adenosine A2a receptors and accumulation of Prostaglandin E2 may be involved in the production of strong wakefulness rebound following relatively long treatments (more than 12 h) with Prostaglandin D2 or CGS21680.
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Activation of ventrolateral preoptic neurons by the somnogen Prostaglandin D2
Proceedings of the National Academy of Sciences of the United States of America, 1998Co-Authors: Thomas E Scammell, Dmitry Gerashchenko, Hirotaka Onoe, Clifford B. Saper, Yoshihiro Urade, Osamu HayaishiAbstract:Prostaglandin D2 (PGD2) is an extensively studied sleep-promoting substance, but the neuroanatomical basis of PGD2-induced sleep is only partially understood. To determine potential regions involved in this response, we used Fos immunohistochemistry to identify neurons activated by infusion of PGD2 into the subarachnoid space below the rostral basal forebrain. PGD2 increased nonrapid eye movement sleep and induced striking expression of Fos in the ventrolateral preoptic area (VLPO), a cluster of neurons that may promote sleep by inhibiting the tuberomammillary nucleus, the source of the ascending histaminergic arousal system. Fos expression in the VLPO was positively correlated with the preceding amount of sleep and negatively correlated with Fos expression in the tuberomammillary nucleus. PGD2 also increased Fos immunoreactivity in the basal leptomeninges and several regions implicated in autonomic regulation. These observations suggest that PGD2 may induce sleep via leptomeningeal PGD2 receptors with subsequent activation of the VLPO.
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Molecular mechanism of sleep regulation by Prostaglandin D2
Journal of Lipid Mediators and Cell Signalling, 1996Co-Authors: Yoshihiro Urade, Osamu Hayaishi, Hitoshi Matsumura, Kikuko WatanabeAbstract:Recent biochemical, molecular biological, and pharmacological experiments revealed that Prostaglandin D synthase as well as Prostaglandin D2 circulated in the ventricular system, subarachnoidal space, and extracellular space in the brain. Prostaglandin D2 then interacts with chemosensors or receptors on the ventro-medial surface of the rostral basal forebrain to initiate the signal to promote sleep. Prostaglandin D2 is, therefore, not a typical neurotransmitter but rather a ‘neurohormone’ or an ‘informational substance’ that circulates through the cerebrospinal fluid and transmits certain chemical messages to promote sleep. The mode of communication through the cerebrospinal fluid in the ventricular system and the extracellular space has advantages for global regulation of the brain to induce sleep.
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Nociceptive effects induced by intrathecal administration of Prostaglandin D2, E2, or F2α to conscious mice
Brain Research, 1990Co-Authors: Shigeko Horiguchi, Masayoshi Hyodo, Osamu HayaishiAbstract:The effects of intrathecal administration of Prostaglandins on pain responses in conscious mice were evaluated by using hot plate and acetic acid writhing tests. Prostaglandin D2 (0.5–3 ng/mouse) had a hyperalgesic action on the response to a hot plate during a 3–60 min period after injection. Prostaglandin E2 showed a hyperalgesic effect at doses of 1 pg to 10 ng/mouse, but the effect lasted shorter (3–30 min) than that of Prostaglandin D2. Similar results were obtained by acetic acid writhing tests. The hyperalgesic effect of Prostaglandin D2 was blocked by simultaneous injection of a substance P antagonist (⩾100ng) but not by AH6809, a prostanoid EP1-receptor antagonist. Conversely, Prostaglandin E2-induced hyperalgesia was blocked by AH6809 (⩾500ng) but not by the substance P antagonist. Prostaglandin F2α had little effect on pain responses. These results demonstrate that both Prostaglandin D2 and Prostaglandin E2 exert hyperalgesia in the spinal cord, but in different ways.
Maria G Belvisi - One of the best experts on this subject based on the ideXlab platform.
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Prostaglandin D2 and the role of the dp1 dp2 and tp receptors in the control of airway reflex events
European Respiratory Journal, 2015Co-Authors: Sarah A Maher, Mark A Birrell, John J Adcock, Michael A Wortley, Eric Dubuis, Sara J Bonvini, Megan S Grace, Maria G BelvisiAbstract:Prostaglandin D2 (PGD2) causes cough and levels are increased in asthma suggesting that it may contribute to symptoms. Although the Prostaglandin D2 receptor 2 (DP2) is a target for numerous drug discovery programmes little is known about the actions of PGD2 on sensory nerves and cough. We used human and guinea pig bioassays, in vivo electrophysiology and a guinea pig conscious cough model to assess the effect of Prostaglandin D2 receptor (DP1), DP2 and thromboxane receptor antagonism on PGD2 responses. PGD2 caused cough in a conscious guinea pig model and an increase in calcium in airway jugular ganglia. Using pharmacology and receptor-deficient mice we showed that the DP1 receptor mediates sensory nerve activation in mouse, guinea pig and human vagal afferents. In vivo , PGD2 and a DP1 receptor agonist, but not a DP2 receptor agonist, activated single airway C-fibres. Interestingly, activation of DP2 inhibited sensory nerve firing to capsaicin in vitro and in vivo . The DP1 receptor could be a therapeutic target for symptoms associated with asthma. Where endogenous PGD2 levels are elevated, loss of DP2 receptor-mediated inhibition of sensory nerves may lead to an increase in vagally associated symptoms and the potential for such adverse effects should be investigated in clinical studies with DP2 antagonists. Prostaglandin D2 activates sensory nerves and evokes cough via DP1 receptors
Yi-hao Chen - One of the best experts on this subject based on the ideXlab platform.
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The upregulation of zinc finger protein 670 and Prostaglandin D2 synthase in proliferative vitreoretinopathy
Graefe's Archive for Clinical and Experimental Ophthalmology, 2016Co-Authors: Yi-hao Chen, Yi-chan Wu, Faye Huang, Jentaie Shiea, Pei-chang WuAbstract:Purpose Proteins in the vitreous play an important role on the induction of proliferative vitreoretinopathy (PVR) after retinal detachment. The aim of this study was to investigate the variation of protein patterns in the vitreous of PVR eyes and examine whether differentially expressed protein levels were expressed in experimental PVR retina. Methods Vitreous samples from PVR and macular hole patients were selected for proteomic analysis. The vitreous protein samples were separated by two-dimensional electrophoresis (2-DE). The differentially expressed protein spots in the two groups were excised and subjected to in-gel digestion and identification by electrospray ionization mass spectrometry (ESI-MS) analysis. Two differentially expressed proteins, zinc finger protein 670 (ZFP 670) and Prostaglandin D2 synthase (PGD2S), were further validated by immunohistochemical staining and western blotting analysis in the retina of the experimental rabbit PVR model. Results In proteome analysis of human vitreous samples, five proteins had increased expression in PVR, including zinc finger protein 670 (ZFP 670), Prostaglandin D2 synthase (PGD2S), IgG (Immunoglobulin G) light chain, transthyretin precursor, and haptoglobin precursor. ZFP 670 and PGD2S levels were expressed significantly higher in the experimental PVR retinas than in the control group. Conclusions Levels of ZFP 670 and PGD2S were elevated in the vitreous fluid of patients with PVR. In addition, there were higher expressions of ZFP 670 and PGD2S in the experimental PVR retina. This result will expand our knowledge of pathophysiologic characteristics of PVR, and might be helpful for further developing possible treatment on this disorder.
Yi-chan Wu - One of the best experts on this subject based on the ideXlab platform.
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The upregulation of zinc finger protein 670 and Prostaglandin D2 synthase in proliferative vitreoretinopathy
Graefe's Archive for Clinical and Experimental Ophthalmology, 2016Co-Authors: Yi-hao Chen, Yi-chan Wu, Faye Huang, Jentaie Shiea, Pei-chang WuAbstract:Purpose Proteins in the vitreous play an important role on the induction of proliferative vitreoretinopathy (PVR) after retinal detachment. The aim of this study was to investigate the variation of protein patterns in the vitreous of PVR eyes and examine whether differentially expressed protein levels were expressed in experimental PVR retina. Methods Vitreous samples from PVR and macular hole patients were selected for proteomic analysis. The vitreous protein samples were separated by two-dimensional electrophoresis (2-DE). The differentially expressed protein spots in the two groups were excised and subjected to in-gel digestion and identification by electrospray ionization mass spectrometry (ESI-MS) analysis. Two differentially expressed proteins, zinc finger protein 670 (ZFP 670) and Prostaglandin D2 synthase (PGD2S), were further validated by immunohistochemical staining and western blotting analysis in the retina of the experimental rabbit PVR model. Results In proteome analysis of human vitreous samples, five proteins had increased expression in PVR, including zinc finger protein 670 (ZFP 670), Prostaglandin D2 synthase (PGD2S), IgG (Immunoglobulin G) light chain, transthyretin precursor, and haptoglobin precursor. ZFP 670 and PGD2S levels were expressed significantly higher in the experimental PVR retinas than in the control group. Conclusions Levels of ZFP 670 and PGD2S were elevated in the vitreous fluid of patients with PVR. In addition, there were higher expressions of ZFP 670 and PGD2S in the experimental PVR retina. This result will expand our knowledge of pathophysiologic characteristics of PVR, and might be helpful for further developing possible treatment on this disorder.
