The Experts below are selected from a list of 159 Experts worldwide ranked by ideXlab platform
Giorgio Carmignoto - One of the best experts on this subject based on the ideXlab platform.
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glutamate mediated cytosolic calcium oscillations regulate a pulsatile Prostaglandin Release from cultured rat astrocytes
The Journal of Physiology, 2003Co-Authors: Micaela Zonta, Annalisa Sebelin, Sara Gobbo, Tommaso Fellin, Tullio Pozzan, Giorgio CarmignotoAbstract:The synaptic Release of glutamate evokes in astrocytes periodic increases in [Ca2+]i, due to the activation of metabotropic glutamate receptors (mGluRs). The frequency of these [Ca2+]i oscillations is controlled by the level of neuronal activity, indicating that they represent a specific, frequency-coded signalling system of neuron-to-astrocyte communication. We recently found that neuronal activity-dependent [Ca2+]i oscillations in astrocytes are the main signal that regulates the coupling between neuronal activity and blood flow, the so-called functional hyperaemia. Prostaglandins play a major role in this fundamental phenomenon in brain function, but little is known about a possible link between [Ca2+]i oscillations and Prostaglandin Release from astrocytes. To investigate whether [Ca2+]i oscillations regulate the Release of vasoactive Prostaglandins, such as the potent vasodilator Prostaglandin E2 (PGE2), from astrocytes, we plated wild-type human embryonic kidney (HEK)293 cells, which respond constitutively to PGE2 with [Ca2+]i elevations, onto cultured astrocytes, and used them as biosensors of Prostaglandin Release. After loading the astrocyte-HEK cell co-cultures with the calcium indicator Indo-1, confocal microscopy revealed that mGluR-mediated [Ca2+]i oscillations triggered spatially and temporally coordinated [Ca2+]i increases in the sensor cells. This response was absent in a clone of HEK cells that are unresponsive to PGE2, and recovered after transfection with the InsP3-linked prostanoid receptor EP1. We conclude that [Ca2+]i oscillations in astrocytes regulate Prostaglandin Releases that retain the oscillatory behaviour of the [Ca2+]i changes. This finely tuned Release of PGE2 from astrocytes provides a coherent mechanistic background for the role of these glial cells in functional hyperaemia.
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Glutamate‐mediated cytosolic calcium oscillations regulate a pulsatile Prostaglandin Release from cultured rat astrocytes
The Journal of Physiology, 2003Co-Authors: Micaela Zonta, Annalisa Sebelin, Sara Gobbo, Tommaso Fellin, Tullio Pozzan, Giorgio CarmignotoAbstract:The synaptic Release of glutamate evokes in astrocytes periodic increases in [Ca2+]i, due to the activation of metabotropic glutamate receptors (mGluRs). The frequency of these [Ca2+]i oscillations is controlled by the level of neuronal activity, indicating that they represent a specific, frequency-coded signalling system of neuron-to-astrocyte communication. We recently found that neuronal activity-dependent [Ca2+]i oscillations in astrocytes are the main signal that regulates the coupling between neuronal activity and blood flow, the so-called functional hyperaemia. Prostaglandins play a major role in this fundamental phenomenon in brain function, but little is known about a possible link between [Ca2+]i oscillations and Prostaglandin Release from astrocytes. To investigate whether [Ca2+]i oscillations regulate the Release of vasoactive Prostaglandins, such as the potent vasodilator Prostaglandin E2 (PGE2), from astrocytes, we plated wild-type human embryonic kidney (HEK)293 cells, which respond constitutively to PGE2 with [Ca2+]i elevations, onto cultured astrocytes, and used them as biosensors of Prostaglandin Release. After loading the astrocyte-HEK cell co-cultures with the calcium indicator Indo-1, confocal microscopy revealed that mGluR-mediated [Ca2+]i oscillations triggered spatially and temporally coordinated [Ca2+]i increases in the sensor cells. This response was absent in a clone of HEK cells that are unresponsive to PGE2, and recovered after transfection with the InsP3-linked prostanoid receptor EP1. We conclude that [Ca2+]i oscillations in astrocytes regulate Prostaglandin Releases that retain the oscillatory behaviour of the [Ca2+]i changes. This finely tuned Release of PGE2 from astrocytes provides a coherent mechanistic background for the role of these glial cells in functional hyperaemia.
John Quilley - One of the best experts on this subject based on the ideXlab platform.
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fenofibrate treatment of diabetic rats reduces nitrosative stress renal cyclooxygenase 2 expression and enhanced renal Prostaglandin Release
Journal of Pharmacology and Experimental Therapeutics, 2008Co-Authors: Yujung Chen, John QuilleyAbstract:Renal cyclooxygenase (COX)-2 expression is increased in the diabetic rat and has been linked to increased glomerular filtration rate (GFR) and renal injury. Our studies indicate that oxidative stress in the form of peroxynitrite (ONOO) may be the stimulus for induction of COX-2. In this study, we addressed the effects of a peroxisome proliferator-activated receptor α agonist on renal COX-2 expression as fibrates exert renal protective effects. Forty-eight hours after the induction of diabetes with streptozotocin in male Wistar rats, fenofibrate treatment (100 mg/kg/day) was started, and the effects were compared with untreated diabetic rats and treated and untreated age-matched control rats ( n = 5 per group). After 12 to 14 weeks of treatment, the right kidney was perfused to determine Prostaglandin Release in response to arachidonic acid (AA), and the left kidney was used to examine the expression of COX-2 and nitrotyrosine, an index of ONOO formation. Release of Prostaglandin (PG) E2 in response to AA was enhanced in the diabetic rat kidney compared with control (4.8 ± 0.7 versus 1.9 ± 0.7 ng/min) and reduced by fenofibrate to 0.6 ± 0.2 ng/min. A similar pattern was obtained for AA-stimulated Release of 6-ketoPGF1α. The effects of fenofibrate were associated with reduced renal expression of COX-2 and nitrotyrosine in diabetic rats. We used creatinine clearance as an index of GFR, which was increased in the diabetic rat, 3.09 ± 0.4 versus 1.15 ± 0.1 ml/min for control, and reduced by fenofibrate treatment to 1.87 ± 0.3 ml/min. These results show that fenofibrate treatment of diabetic rats decreases renal COX-2 expression, possibly by reducing nitrosative stress, and is associated with a reduction of the enhanced GFR.
Guido Franceschini - One of the best experts on this subject based on the ideXlab platform.
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high density lipoproteins protect isolated rat hearts from ischemia reperfusion injury by reducing cardiac tumor necrosis factor α content and enhancing Prostaglandin Release
Circulation Research, 2003Co-Authors: Laura Calabresi, Giuseppe Rossoni, Monica Gomaraschi, Francesca Sisto, F Berti, Guido FranceschiniAbstract:The incidence and severity of primary cardiac events are inversely related to the plasma concentration of high-density lipoproteins (HDLs). We investigated whether HDLs may exert a direct cardioprotection in buffer-perfused isolated rat hearts, which underwent a 20-minute low-flow ischemia followed by a 30-minute reperfusion. The administration of HDLs at physiological concentrations (0.5 and 1.0 mg/mL) during the 10 minutes immediately before ischemia rapidly and remarkably improved postischemic functional recovery and decreased creatine kinase Release in the coronary effluent. Reconstituted HDLs containing apolipoprotein A-I (apoA-I) and phosphatidylcholine, but not lipid-free apoA-I or phosphatidylcholine liposomes, were also effective in protecting the heart from ischemia-reperfusion injury. HDLs at reperfusion were less effective than when given before ischemia. HDLs caused a dose-dependent reduction of ischemia-induced cardiac tumor necrosis factor-α (TNF-α) expression and content, which correlated with the improved functional recovery. A parallel increase of TNF-α Release in the coronary effluent was observed, due to a direct binding of cardiac TNF-α to HDLs. Taken together, these findings argue for a cause-effect relationship between the HDL-mediated removal of TNF-α from the ischemic myocardium and the HDL-induced cardioprotection. Indeed, etanercept, a recombinant TNF-α–blocking protein, caused a dose-dependent improvement of postischemic functional recovery. HDLs also enhanced ischemia-induced Prostaglandin Release, which may contribute to the cardioprotective effect. A low plasma HDL level may expose the heart to excessive ischemia-reperfusion damage, and HDL-targeted therapies may be helpful to induce immediate or delayed myocardial protection from ischemia-reperfusion injury.
Burkhard H Dick - One of the best experts on this subject based on the ideXlab platform.
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nsaid pretreatment inhibits Prostaglandin Release in femtosecond laser assisted cataract surgery
Journal of Refractive Surgery, 2015Co-Authors: Tim Schultz, Stephanie C Joachim, Marek Szuler, Mathias Stellbogen, Burkhard H DickAbstract:PURPOSE: To investigate whether short-term nonsteroidal anti-inflammatory drug (NSAID) pretreatment on the day of surgery inhibits Prostaglandin Release. Previous studies detected elevated Prostaglandin levels after femtosecond laser treatment and identified them as a potential mediator for laser-induced miosis. METHODS: Patients underwent either image-guided femtosecond laser cataract surgery or conventional cataract surgery (n = 75). Half of the eyes per group received topical NSAID treatment on the day of surgery. Aqueous humor was collected from all patients. ELISA measurements were performed to detect aqueous humor Prostaglandin levels. RESULTS: Femtosecond laser cataract surgery led to higher Prostaglandin levels than conventional cataract surgery (P = .007). In both groups, NSAID pretreatment led to reduced Prostaglandin Release. In the femtosecond laser group, patients pretreated with NSAIDs had significantly lower Prostaglandin values (65.3 ± 13.2 pg/mL) than patients not pretreated with NSAIDs (294.4 ± 66.5 pg/mL) (P = .0009). CONCLUSIONS: The short-term NSAID treatment prevented Prostaglandin Release in patients treated with image-guided femtosecond laser. Therefore, it has potential to limit intraoperative laser-induced miosis.
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Prostaglandin Release during femtosecond laser assisted cataract surgery main inducer
Journal of Refractive Surgery, 2015Co-Authors: Tim Schultz, Stephanie C Joachim, Mathias Stellbogen, Burkhard H DickAbstract:PURPOSE: To investigate a possible correlation between intraocular Prostaglandin concentrations and partial steps of laser-assisted cataract surgery. METHODS: Aqueous humor was collected from 67 patients after laser-assisted cataract surgery pretreatment (only capsulotomy, only fragmentation, or both) and at the beginning of routine cataract surgery. Total Prostaglandin levels were measured in all four groups using an enzyme-linked immunoassay. RESULTS: Significantly higher levels of aqueous humor Prostaglandins were detected right after the full treatment (capsulotomy and fragmentation [330.6 ± 110.6 pg/mL; P = .01] or only laser capsulotomy [362.4 ± 117.5 pg/mL; P = .01]), whereas the control group showed lower values (52.5 ± 8.1 pg/mL). By itself, laser-assisted cataract surgery fragmentation did not lead to a Prostaglandin increase (186.8 ± 114.0 pg/mL; P = .14). CONCLUSIONS: This study identified the anterior capsulotomy as the main trigger for an increase of Prostaglandins in the aqueous humor immediately after laser-assisted cataract surgery. Optimized energy settings in combination with nonsteroidal anti-inflammatory drugs might help reduce the phenomenon of laser-induced miosis.
Micaela Zonta - One of the best experts on this subject based on the ideXlab platform.
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glutamate mediated cytosolic calcium oscillations regulate a pulsatile Prostaglandin Release from cultured rat astrocytes
The Journal of Physiology, 2003Co-Authors: Micaela Zonta, Annalisa Sebelin, Sara Gobbo, Tommaso Fellin, Tullio Pozzan, Giorgio CarmignotoAbstract:The synaptic Release of glutamate evokes in astrocytes periodic increases in [Ca2+]i, due to the activation of metabotropic glutamate receptors (mGluRs). The frequency of these [Ca2+]i oscillations is controlled by the level of neuronal activity, indicating that they represent a specific, frequency-coded signalling system of neuron-to-astrocyte communication. We recently found that neuronal activity-dependent [Ca2+]i oscillations in astrocytes are the main signal that regulates the coupling between neuronal activity and blood flow, the so-called functional hyperaemia. Prostaglandins play a major role in this fundamental phenomenon in brain function, but little is known about a possible link between [Ca2+]i oscillations and Prostaglandin Release from astrocytes. To investigate whether [Ca2+]i oscillations regulate the Release of vasoactive Prostaglandins, such as the potent vasodilator Prostaglandin E2 (PGE2), from astrocytes, we plated wild-type human embryonic kidney (HEK)293 cells, which respond constitutively to PGE2 with [Ca2+]i elevations, onto cultured astrocytes, and used them as biosensors of Prostaglandin Release. After loading the astrocyte-HEK cell co-cultures with the calcium indicator Indo-1, confocal microscopy revealed that mGluR-mediated [Ca2+]i oscillations triggered spatially and temporally coordinated [Ca2+]i increases in the sensor cells. This response was absent in a clone of HEK cells that are unresponsive to PGE2, and recovered after transfection with the InsP3-linked prostanoid receptor EP1. We conclude that [Ca2+]i oscillations in astrocytes regulate Prostaglandin Releases that retain the oscillatory behaviour of the [Ca2+]i changes. This finely tuned Release of PGE2 from astrocytes provides a coherent mechanistic background for the role of these glial cells in functional hyperaemia.
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Glutamate‐mediated cytosolic calcium oscillations regulate a pulsatile Prostaglandin Release from cultured rat astrocytes
The Journal of Physiology, 2003Co-Authors: Micaela Zonta, Annalisa Sebelin, Sara Gobbo, Tommaso Fellin, Tullio Pozzan, Giorgio CarmignotoAbstract:The synaptic Release of glutamate evokes in astrocytes periodic increases in [Ca2+]i, due to the activation of metabotropic glutamate receptors (mGluRs). The frequency of these [Ca2+]i oscillations is controlled by the level of neuronal activity, indicating that they represent a specific, frequency-coded signalling system of neuron-to-astrocyte communication. We recently found that neuronal activity-dependent [Ca2+]i oscillations in astrocytes are the main signal that regulates the coupling between neuronal activity and blood flow, the so-called functional hyperaemia. Prostaglandins play a major role in this fundamental phenomenon in brain function, but little is known about a possible link between [Ca2+]i oscillations and Prostaglandin Release from astrocytes. To investigate whether [Ca2+]i oscillations regulate the Release of vasoactive Prostaglandins, such as the potent vasodilator Prostaglandin E2 (PGE2), from astrocytes, we plated wild-type human embryonic kidney (HEK)293 cells, which respond constitutively to PGE2 with [Ca2+]i elevations, onto cultured astrocytes, and used them as biosensors of Prostaglandin Release. After loading the astrocyte-HEK cell co-cultures with the calcium indicator Indo-1, confocal microscopy revealed that mGluR-mediated [Ca2+]i oscillations triggered spatially and temporally coordinated [Ca2+]i increases in the sensor cells. This response was absent in a clone of HEK cells that are unresponsive to PGE2, and recovered after transfection with the InsP3-linked prostanoid receptor EP1. We conclude that [Ca2+]i oscillations in astrocytes regulate Prostaglandin Releases that retain the oscillatory behaviour of the [Ca2+]i changes. This finely tuned Release of PGE2 from astrocytes provides a coherent mechanistic background for the role of these glial cells in functional hyperaemia.
